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How does vasoconstriction/vasodilation change blood pressure?

How does vasoconstriction/vasodilation change blood pressure?


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Background: I am coming at this question from an electrical engineering background, and I feel like I am missing certain assumptions that are going into the statement found in my physiology textbook, "vasoconstriction increases blood pressure"."

Consider a simple series circuit and a parallel circuit run by a battery/heart [you will find the parallel and series circuit in any physiology book description of the vasculature, yet I can't find any exploration of the assumptions made when applying these circuit models]:

  1. In the series circuit, if I have an increase in resistance across one of my resistors, this will basically redistribute the pressure drops across the resistors, but it will not alter the total pressure drop across all the resistors [fixed by the heart].

  2. In the parallel circuit, if I have an increase in resistance across one of my resistors, this will redistribute the flow to different branches, but the pressure drop will not change as again this is fixed by the heart.

This analysis seems to suggest that if the resistance across an organ [branch of parallel circuit] changes, the flow changes, not the pressure. The heart, I would assume, then responds by increasing the pressure to increase flow ie actually injecting energy into the system.

Here is the problem with the circuit model though:

  1. it assumes that the battery/heart is the only source of energy in the system, and the resistors are passive re distributors of that energy.

    the controllers of vascular resistance are smooth muscle which must actively put energy into the system to vasoconstrict. This could be a source of pressure increase as the smooth muscle would be actively constricting against an incompressible fluid, but I am really not sure.

  2. it does not account for the compliance of the vasculature.

-the tubing the heart is hooked up to modifies the blood pressure the heart has to generate to inject fluid into that tube. If the tubing was stiff, the heart would have to generate very high systolic pressures that would then rapidly decrease during the diastolic phase. The more compliant the tubing, the less pressure the heart has to generate to inject fluid into the tube. Intuitively though, there would seem to some relationship between the ability of a fluid to flow and vessel compliance. A highly compliant vessel with a fluid injection will simply expand and hold the fluid while a less compliant vessel will maintain a pressure necessary to push the fluid along.

Sparknotes in the form of questions:

  1. Is the only source of energy in the cardiac circuit the heart? Or does artiole smooth muscle actually inject energy into the system, and result in systemic increases in the pressure available in the closed circuit.

  2. I don't think vascular compliance ie expansion of the artery walls due to volume filling results in any active injections of energy into the system… it should simply transfer the energy available to push fluid to elastic energy in the connective tissue of the artery walls. Is this correct?

  3. Does vessel compliance partly determine the pressure the heart has to inject into the system?

  4. What is the relationship between compliance and flow if there is one?

The circulatory system is a dynamic system which cannot be adequately explained by your example (at least not by me). You need to understand it, not seek to make it fit your (especially) electrical circuits with resistors. Blood isn't electricity. At least try a fluid dynamics model.

Let's take this very simple model: Blow up a balloon four-fifths of the way, and put a wide inflatable cuff around its middle. Inflate the cuff so that the balloon bulges just a tiny bit at the ends, then stuff it all into a plexiglass box so that the balloon has no room to expand. The plexiglass box represents our body. Lets call the pressure inside the balloon now normal blood pressure. The air in the balloon represents your total blood volume. It can't change from moment to moment; it's fixed. The box can't change it's volume moment to moment either. It's fixed.

The cuff represents arterial smooth muscle. Vasoconstriction can be represented by inflating the cuff further. Constriction (inflation of the cuff) will increase the pressure throughout inside the balloon, because the same amount of gas now has to exist in a smaller space. Vasodilation (deflating the cuff) decreases the pressure inside the balloon, because the gas can now inhabit a larger amount of space.

That's it, really. If the same volume must inhabit a smaller, constricted space, the pressure exerted by blood in that space will be higher. If the blood vessles dilate, the pressure in the blood vessels falls.

Now add about 20 layers of complexity to that simple model, and you have a working model of the circulatory system.

Sparknote answers:

  1. Arterial and arteriolar smooth muscle "injects energy into the system", resulting in systemic increases in the pressure existing in the vascular "circuit" (meaning somewhat elastic tubing) if resistance requires energy. (So I have misunderstood: see @Raoul's answer.)

  2. Sorry, I didn't read this properly the first time around. Yes, the heart supplies the energy. The contribution of the elastic walls of the arteries is not active, but passive.

  3. Absolutely. The more elastic/compliant the arteries are, the less work the heart must exert to pump the blood through the circuits. The stiffer and narrower the arteries are, the harder the heart must work to pump blood through the circuits. The result of that increased work is a thickening of the muscular walls of the heart, called ventricular hypertrophy, which is a sign of elevated pressure in the system.

  4. I'm not sure I want to commit here to your lingo, but the answer should be inferable from numbers 1-3. Elastic vessels help (by rebound compression) to propel the blood through the circuits. Stiff vessels hinder it, making the heart do more of the work.

I am not an engineer, so I may be misusing some of the terms.

Edited to add: Please see @Raoul's answer for a better explanation.


I'll try a brief answer myself.

  1. No, the heart is not the only energy provider, as others have stated above. Does vasoconstriction inject energy into the system? Not really. Arteriolar constriction will increase the resistance of the system. Therefore, more energy will be required to keep flow at a constant level when vasocontriction occurs. Arteriolar vasoconstriction forces the system to function at a higher energy level, yet it does not inject energy targeted at facilitating flow.

  2. Yes, your assumption is correct.

  3. @anongoodnurse answered correctly.

  4. There is no direct relationship between compliance and flow. They are independent factors. The important point is the following: during diastole, the heart is isolated from the vessels. The higher the vessel compliance is, the more potential elastic energy will be transferred from the heart to the vessels during systole, to then ensure good flow during diastole. In elderly persons for example, arteries are usually stiff, systolic pressure is high, and diastolic pressure is low (as is flow).

To conclude, I would say that the most important lesson that is to be learned here is that although a higher blood pressure means a higher energy state and more work for the heart, it is incorrect to assume that blood flow is physiologically adequate because pressure is high! This is a common mistake made in the emergency room.


I just want to add a few points to the above answer:

Heart is not the only organ which helps blood flow. The following structures also help:

  • The action of muscles on deep veins acts as a pump - Soleus is called peripheral heart for that matter
  • The compliance itself adds to the flow - Infact the compliance of the blood vessels is what makes the blood flow continuous instead of pulsatile like a system with stiff tubes would be expected to act when the pump is pulsatile in nature

Some Critical Points to keep in mind:

  1. The circulatory system is made in such a way that the total sum of cross sections of all the vessels at a particular level is as follows:

    • The sumtotal of cross-sections of all capillaries is the largest cross section ~ 11308 cm2, (approximately only 1/4 are open under normal pressure, so effective cross section is ~ 2827 cm2)
    • The sumtotal of cross-sections of venules followed by arterioles (~141 cm2) (venules more than arterioles as arterioles normally are under a tonal contraction)
    • Sumtotal of cross-sections of veins followed by arteries (~63 cm2)
    • Cross-section of Vena Cava ~ 1.38 cm2 followed by Aorta ~ 1.13 cm2

      So if the cross sections are added up: Capillaries > Venules > Arterioles > Veins > Arteries

  2. The Pressure Blood Pressure we measure is not exactly the flow pressure aka the pressure gradient. We measure the radial pressure not the pressure gradient. Special equipment is needed to measure pressure gradient.

  3. The volume of fluid inside a parallel circuit (artery to capillary to vein) is not constant as plasma diffuses out at the small arterioles and capillary levels and diffuses back in at the venous side.

  4. The pressure flow curve is not linear due to the compliance of the blood vessels.

  5. The heart contributes very little to the blood flow in the veins. (To re emphasize that heart is not the only organ driving circulation). It is mainly through postural drainage and muscle action.

Coming to your question I like to point out one thing:

If there is a need to increase perfusion, the vasoconstriction occurs at the venular side. The capillary pressure is responsible for perfusion.

$$P_c = frac{(R_{post}/R_{pre}).P_a + P_v}{1 + (R_{post}/R_{pre})}$$ Where P - pressure and the characters a, v and c denotes artery, vein and capillary resistance

Rpost - Post-capillary resistance

Rpre - Pre-capillary resistance

The equation and picture are taken from Boron and Boulpaep textbook of Medical Physiology, 2nd Edition, Chapter 19: Arteries and Viens.

When there is a need to increase the perfusion to an organ the post capillary pressure is raised by venoconstiction (or in the case of glomeruli of kidney constriction of efferent arterioles). As you can see from the above equation, such a rise will cause rise in the capillary pressure and increase the perfusion.

Otherwise vasoconstriction occurs to do exactly what you assumed would happen: to redirect blood flow. In fact this happens at several levels:

  1. Vasoconstriction of periphery (limbs) occur in cold conditions which causes cyanosis (meaning the flow is so reduced that most oxygen is used up)
  2. Vasoconstriction of Splanchnic vessels occur when muscles need more blood (during exercise, flight, fight, etc… )

If you can read this chapter you will understand the equation much better. This book explains the physics behind physiology in a beautiful manner.


Difference Between Vasodilation and Vasoconstriction

Warm-blooded animals are capable of regulating their body temperature independently from the environmental temperature. Vasoconstriction and vasodilation are the two types of mechanisms involved in the thermoregulation in the above-mentioned animals. The main difference between vasodilation and vasoconstriction is that vasodilation is the widening of blood vessels whereas vasoconstriction is the narrowing of blood vessels. Both vasodilation and vasoconstriction occur under the influence of the nervous system. Smooth muscles are responsible for both vasodilation and vasoconstriction.

Key Areas Covered

Key Terms: Blood Capillaries, Blood Vessels, Smooth Vessels, Vasoconstriction, Vasoconstrictors, Vasodilation, Vasodilators


It is important to understand the concept of cardiac output, stroke volume, preload, Frank-Starling law, afterload, and ejection fraction to understand the physiology of the heart. The cardiac output (CO) is the amount of blood ejected from the left ventricle, and normally it is equal to the venous return. The calculation is CO = stroke volume (SV) x heart rate (HR). CO also equals the rate of oxygen consumption divided by the difference in arterial and venous oxygen content. The stroke volume is the amount of blood pumped out of the heart after one contraction. It is the difference in end-diastolic (EDV) and end-systolic volume (ESV). It increases with increased contractility, increased preload, and decreased afterload. Also, contractility of the left ventricle increases with catecholamines by increasing intracellular calcium ions and lowering extracellular sodium. The preload is the pressure on the ventricular muscle by the ventricular EDV. Frank-Starling law describes the relationship between EDV and SV. This law states that the heart attempts to equalize CO with venous return. As venous return increases, there is a larger EDV in the left ventricle, which leads to further stretching of the ventricle. Further stretching of the ventricle leads to a larger contraction force and a larger SV. A larger stroke volume leads to a larger CO, thus equalizing CO with venous return. Next, the afterload is the pressure that the left ventricular pressure must exceed to push blood forward. Mean arterial pressure best estimates this. Also, afterload can be estimated by the minimum amount of pressure needed to open the aortic valve, which is equivalent to the diastolic pressure. Thus, diastolic blood pressure is one of the better ways to index afterload. Finally, the ejection fraction (EF) is equal to SV/EDV. EF of the left ventricle is an index for contractility. A normal EF is greater than 55%. A low EF indicates heart failure.[4][5][6][7]

The cardiac cycle describes the path of the blood through the heart. It runs in the following order:

Vasculature plays a significant role in the regulation of blood flow throughout the body. In general, blood pressure decreases from arteries to veins, and this is because of the pressure overcoming the resistance of the vessels. The greater the change in resistance at any point in the vasculature, the greater the loss of pressure at that point. Arterioles have the most increase in resistance and cause the largest decrease in blood pressure. The constriction of arterioles increases resistance, which causes a decrease in blood flow to downstream capillaries and a larger decrease in blood pressure. Dilation of arterioles causes a decrease in resistance, increasing blood flow to downstream capillaries, and a smaller decrease in blood pressure. Diastolic blood pressure (DP) is the lowest pressure in an artery at the beginning of the cardiac cycle, while the ventricles are relaxing and filling. DP is directly proportional to total peripheral resistance (TPR). Also, the energy stored in the compliant aorta during systole is now released by the recoil of the aortic wall during diastole, thus increasing diastolic pressure. Systolic blood pressure (SP) is the peak pressure in an artery at the end of the cardiac cycle, while the ventricles are contracting. Directly related to stroke volume, as stroke volume increases, SP also increases. SP is also affected by aortic compliance. Because the aorta is elastic, it stretches and stores the energy caused by ventricular contraction and decreases the systolic pressure. Pulse pressure is the difference between SP and DP. Pulse pressure is proportional to SV and inversely proportional to arterial compliance. Thus the stiffer the artery, the larger the pulse pressure. Mean arterial pressure (MAP) is the average pressure in the arteries throughout the cardiac cycle. The MAP is always closer to DP. MAP is calculated by MAP= DP + 1/3 (pulse pressure). Also, by MAP = CO x TPR, where CO is cardiac output. This value is significant because whenever there is a decrease in CO, to maintain the MAP, the TPR will increase, which is relevant in many pathophysiology problems.

Systemic veins have a lower decrease in pressure because it has low resistance. The venous system is very compliant contains up to 70% of the circulating blood at once. A small change in venous pressure can mobilize the blood stored in the venous system. Velocity of blood in the vasculature has an inverse relationship with cross-sectional area (volumetric flow rate (Q) = flow velocity (v) x cross-sectional area (A)). As the cross-sectional area increases, velocity decreases. Arteries and veins have smaller cross-sectional areas and the highest velocities, whereas capillaries have the most cross-sectional area and the lowest velocities. The vasculature also gives resistance. Resistance is R= (8*viscosity*length)/(πr^4). Viscosity depends on hematocrit and increases in multiple myeloma or polycythemia. As tube length increases, the resistance increases. As tube radius increases, the resistance decreases. The fact that the radius is to the power of 4 means that slight changes in the radius have a profound effect on resistance. The total resistance of vessels in a series is R1 + R2 + R3, and so on, and the total resistance of arteries in parallel is 1/TR = 1/R1+1/R2+1/R and so on, where TR is the total resistance.

The Poiseuille equation measures the flow of blood through a vessel. It is measured by the change in pressure divided by resistance: Flow = (P1 - P2)/R, where P is pressure, and R is resistance. Increasing resistance in a vessel, such as the constriction of an arteriole, causes a decrease in blood flow across the arteriole. At the same time, there is a larger decrease in pressure across this point because the pressure is lost by overcoming the resistance. Increasing the resistance at any point increases upstream pressure but decreases downstream pressure. The Poiseuille equation applies to the systemic circulation such that F is the cardiac output (CO), P1 is the mean arterial pressure (MAP), P2 is the right atrial pressure (RAP), and R is the total peripheral resistance (TPR). Because RAP is close to 0 and very small in comparison to MAP, the equation approximates as F=P1/R or CO=MAP/TPR where MAP=CO*TPR - this means that cardiac output and total peripheral resistance control MAP. Its application is important, because in trauma situations with hemorrhage, there is also a decrease in cardiac output, but at times the blood pressure is near normal, this is because the TPR at the level of the arterioles has increased. This equation, as applied to the pulmonary vasculature, is used to determine the cause of pulmonary hypertension. As related to the pulmonary vasculature F represents CO, P1 represents pulmonary artery pressure (PAP), and P2 represents left atrial pressure (LAP), and R is pulmonary vascular resistance (PR) CO=(PAP-LAP)/PR. A Swan-Ganz catheter helps to measure both PAP and LAP, allowing for the measurement of PR and, thus, the etiology of pulmonary hypertension.

The nervous system regulates the cardiovascular system with the help of baroreceptors and chemoreceptors. Both receptors are located in the carotids and aortic arch. Also, both have afferent signals through the vagus nerve from the aortic arch and afferent signals through the glossopharyngeal nerve from the carotids.

Autoregulation is the method by which an organ or tissue maintains blood flow despite a change in perfusion pressure. When blood flow becomes decreased to an organ, arterioles dilate to reduce resistance.

The starling equation can explain the capillary fluid exchange. This਎quation describes the forces of oncotic and hydrostatic pressure on the movement of fluid across the capillary membrane. Edema can result from an increase in capillary pressure (heart failure), a decrease in plasma proteins (liver failure), an increase in the interstitial fluid due to lymphatic blockage, or an increase in capillary permeability due to infections or burns.


How does vasoconstriction/vasodilation change blood pressure? - Biology

The sympathetic nervous system can cause perspiration (sweating), widen blood vessels (vasodilation), and constrict blood vessels (vasoconstriction).

The sympathetic nervous system (SNS) aids in the control of most of the body’s internal organs. It is responsible for regulating many homeostatic mechanisms in living organisms, including the skin. The SNS is perhaps best known for mediating the neuronal and hormonal stress response commonly known as the fight-or-flight response, also known as sympatho-adrenal response of the body. This occurs as the preganglionic sympathetic fibers that end in the adrenal medulla secrete acetylcholine, which activates the secretion of adrenaline (epinephrine), and to a lesser extent noradrenaline (norepinephrine).

This response is mediated directly via impulses transmitted through the sympathetic nervous system, and also indirectly via catecholamines that are secreted from the adrenal medulla. Messages travel through the SNS in a bidirectional flow. Efferent messages can trigger simultaneous changes in different parts of the body. For example, the sympathetic nervous system can cause perspiration (sweating), widen blood vessels (vasodilation), and constrict blood vessels (vasoconstriction).

Perspiration, or sweating, is the production of fluids secreted by the sweat glands in the skin of mammals. Two types of sweat glands can be found in humans: eccrine glands and apocrine glands. Eccrine glands are the major sweat glands of the human body, found in virtually all skin. They produce a clear, odorless substance consisting primarily of water and NaCl (note that the odor from sweat is due to bacterial activity on the secretions of the apocrine glands). NaCl is reabsorbed in the duct to reduce salt loss. Eccrine glands are active in thermoregulation and are stimulated by the sympathetic nervous system. This involuntary increase in sweating increases skin conductivity, which is an indication of psychological and physiological arousal.

Apocrine sweat glands are inactive until they are stimulated by hormonal changes in puberty. Apocrine sweat glands are mainly thought to function as olfactory pheromones, chemicals important in attracting a potential mate. The stimulus for the secretion of apocrine sweat glands is adrenaline, which is a hormone carried in the blood.

The secretion of medullary epinephrine and norepinephrine is controlled by a neural pathway that originates from the hypothalamus in response to danger or stress (the SAM pathway). Both epinephrine and norepinephrine signal the liver and skeletal muscle cells to convert glycogen into glucose, resulting in increased blood glucose levels. These hormones increase the heart rate, pulse, and blood pressure to prepare the body to fight the perceived threat or flee from it. In addition, the pathway dilates the airways, raising blood oxygen levels. It also prompts vasodilation, further increasing the oxygenation of important organs such as the lungs, brain, heart, and skeletal muscle. At the same time, it triggers vasoconstriction to blood vessels serving less essential organs such as the gastrointestinal tract, kidneys, and skin, and downregulates some components of the immune system. Other effects include a dry mouth, loss of appetite, pupil dilation, and a loss of peripheral vision.


Practice Questions


Khan Academy

MCAT Official Prep (AAMC)

Biology Question Pack, Vol 2. Passage 17 Question 110

Section Bank B/B Section Passage 1 Question 4

Practice Exam 4 Passage 1 Question 3

Practice Exam 4 B/B Section Passage 8 Question 40


Key Points

• Eccrine glands, the major sweat glands of the human body, produce a clear, odorless substance, consisting primarily of water and NaCl. NaCl is reabsorbed in the duct to reduce salt loss.

• Apocrine sweat glands are found only in certain locations of the body: the axillae (armpits), areola and nipples of the breast, ear canal, perianal region, and some parts of the external genitalia.

• Increased adrenaline stimulates the apocrine glands for sweating.

• The hormone epinephrine can cause both vasoconstriction and vasodilation.

Perspiration (sweating): The production of fluids secreted by the sweat glands in the skin of mammals

Apocrine: Secretion in the form of membrane-bound vesicles.

Vasodilation: The dilatation of blood vessels, which decreases blood pressure.

Vasoconstriction: The narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels.

Sympathetic nervous system (SNS): Part of the autonomic nervous system (ANS). The sympathetic nervous system activates what is often termed the fight or flight response.

Adrenaline (epinephrine): A hormone secreted by the adrenal glands, especially in conditions of stress, increasing rates of blood circulation, breathing, and carbohydrate metabolism and preparing muscles for exertion.

Noradrenaline (norepinephrine): A substance that is released predominantly from the ends of sympathetic nerve fibres and that acts to increase the force of skeletal muscle contraction and the rate and force of contraction of the heart.


Which Category of Vascular Migraines Are You In?

Below is a list of the symptoms that may help you identify your type of vascular migraine. Talk to your doctor if you experience several of them so that he or she can properly diagnose it and prescribe medications to treat and prevent the attacks.

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Vasodilatory headaches

Your headaches may be caused by vasodilation if it occurs as a result of:

  • Heat
  • Sex and masturbation (both vasodilators)
  • Exercise (during or post)
  • An infection or sickness
  • An injury
  • Ingestion any food or chemical that they are sensitive to (gluten, casein, etc..)
  • Hypoglycemia
  • MSG
  • Hot flushes by perimenopausal women (increases vasodilation from estrogen) Estrogen also fluctuates in pregnancy and menarche
  • After menstruation &ndash estrogen levels peak

Exercise, infection, injury and food intolerances may cause inflammation, which leads to vasodilation.

People will usually, but not always, have lower than average blood pressure because vasodilation lowers blood pressure.

MSG or excess glutamine/glutamic acid consumption can worsen vasodilatory migraines because glutamate excess causes vasodilation. The degree of harm caused by MSG is probably minimal.

Instead, glutamate excess is more likely caused by a host of other factors not related to dietary consumption of glutamates such as hypoglycemia caused by eating high glycemic index foods, hyperinsulinemia, fasting/skipping meals or really low carb dieting.

Also, low oxygen can cause glutamate excitotoxicity, such as when we are so stressed we forget to breathe, but more likely as a result of sleep apnea (if you get a headache in the morning check for sleep apnea).

Vasodilatory headaches are least responsive to nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin because while aspirin will block the pain to a certain extent and bring down inflammation, it is a vasodilator itself. So in one way, it makes it better (by decreasing inflammation) and in another, it exacerbates the problem (by increasing vasodilation). If your headaches don&rsquot improve with aspirin, that&rsquos another indicator that it&rsquos caused by vasodilation.

NSAIDs have been shown not to work for vasodilatory headaches like cluster or exercise headaches because NSAIDs vasodilatory actions will only help for vasoconstrictive headaches.

Allergies and allergic reactions cause an inflammatory response which will trigger or make this headache worse.

Vasoconstriction headaches

People with vasoconstriction headaches will usually have higher blood pressure and experience episodes during times of stress. Tension headaches are a good example of this.

Stress and tyramines, for example, can trigger vasoconstriction. Stress triggers vasoconstriction through cortisol, epinephrine, and norepinephrine.

Any stimulus that causes the body to release stress hormones such as fasting or skipping meals, emotional stress, cold, bright lights, and loud noise can aggravate these headaches.

Tyramines, found in aged cheeses and other foods, displace norepinephrine from neuronal storage vesicles, which leads to vasoconstriction. These headaches can come often but they aren&rsquot as consistent as vasodilatory headaches.

These headaches are most responsive to NSAIDs like aspirin because aspirin is both a painkiller and vasodilator. And indeed, the research demonstrates its effectiveness for tension headaches.

People with vasoconstricting headaches are more likely to have:

Serotonergic like SSRI&rsquos and tryptophan or foods which contain high levels of tryptophan may increase serotonin levels and possibly exacerbate vasoconstriction headaches

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Structure of Blood Vessels

All blood vessels are basically hollow tubes with an internal space, called a lumen, through which blood flows. The lumen of an artery is shown in cross-section in the photomicrograph below. The width of blood vessels varies, but they all have a lumen. The walls of blood vessels differ depending on the type of vessel. In general, arteries and veins are more similar to one another than capillaries in the structure of their walls.

Figure (PageIndex<6>): The lumen is the white space in the center of this cross-sectional slice of an artery. You can see that the walls of the artery have multiple layers.


Endothelins

Discovery

Vasoconstriction dependent on or enhanced by intact endothelium has been observed in response to various chemical and physical stimuli such as norepinephrine, thrombin, hypoxia, increased transmural pressure, mechanical stretch. These observations lead to the speculation that endothelial cells may release certain vascular constricting substance(s), endothelium-derived contracting factors (EDCF). In 1985, Hickey et al. attempted to test the biological activity of the culture medium of bovine aortic endothelial cells on isolated porcine coronary arteries, and they found that the culture supernatant contained peptide-like factor(s), which triggered a slowly developing and long-lasting contraction of the coronary arteries. Based on gel chromatography analysis, they suggested that this particular EDCF is a peptide with a molecular mass of approximately 8500 Da. 8 At about the same time, Gillespie et al. also detected vascular constricting activity in the culture supernatant of porcine aortic endothelial cells. They subsequently reported that the activity was increased when the cultured endothelial cells were stimulated by thrombin, and they suggested that this EDCF is a peptide with a molecular mass of approximately 3000 Da. 19

In 1987, we performed experiments similar to those of Hickey et al. and confirmed that the supernatant from confluent monolayer cultures of porcine aortic endothelial cells contained a slowly developing and long-lasting vascular constricting factor(s), peptidic in nature, because the vascular constricting activity was abolished by pretreatment of the conditioned medium with trypsin. The activity was also detected in serum-free conditioned medium, and no appreciable change in activity was observed even after long-term (2–3 weeks) maintenance of the endothelial cell culture in serum-free condition. The successful attempt at serum-free maintenance and detection of vascular constricting activity prompted us to isolate and purify the active peptide in the supernatant because of the absence of interference with proteins and/or peptides in the serum itself.

Cells isolated from porcine thoracic aortas and grown to a confluent monolayer were maintained in serum-free minimum essential medium. The medium was changed every 5 days, and the conditioned medium was pooled at −20 °C. The pooled conditioned medium was first centrifuged at 1000 g for 20 min, and subsequently, the supernatant was desalted and concentrated. The concentrated medium was loaded onto an anion-exchange column and eluted by applying a linear gradient of NaCl. The vascular constricting activity of the eluent was assayed by adding a small amount of each fraction directly into a muscle chamber where a helical strip of porcine coronary artery with the intima denuded was suspended, and the active fraction was collected. The active fraction was subjected to reversed-phase high-performance liquid chromatography (HPLC) and elution with a linear gradient of acetonitrile, and the vascular constricting activity of each fraction was similarly assayed. A second trial of reversed-phase HPLC enabled us to purify the active component. Approximately 3 nmol of the final product was obtained, which was just enough to perform subsequent amino acid analysis.

The purified peptide was subjected to amino acid sequence analysis by means of an automated gas-phase peptide sequencer and carboxy-terminal analysis by hydrazinolysis (Edman’s reaction). As a result, the peptide was revealed to be composed of 21 amino acid residues with free amino- and carboxy-termini. At first, the carboxy-terminal amino acid (tryptophan) was not detected, and a 20 amino acid peptide synthesized artificially did not exhibit any biological activity. It was soon recognized that the structure of tryptophan (indole ring) is easily degraded during Edman’s reaction. The peptide comprising 21 amino acid residues subsequently synthesized did exhibit vascular constricting activity identical to that of natural peptide. The four cysteine residues at the amino-terminal portion were found to form two intramolecular disulfide bonds, the topological analysis of which revealed that the arrangement of disulfide bonds is a coaxial form (1–15 and 3–11). Because it was originally discovered from the culture supernatant of endothelial cells, the peptide was termed “endothelin.” 27


Autonomic control of body temperature and blood pressure: influences of female sex hormones

Female reproductive hormones exert important non-reproductive influences on autonomic regulation of body temperature and blood pressure. Estradiol and progesterone influence thermoregulation both centrally and peripherally, where estradiol tends to promote heat dissipation, and progesterone tends to promote heat conservation and higher body temperatures. Changes in thermoregulation over the course of the menstrual cycle and with hot flashes at menopause are mediated by hormonal influences on neural control of skin blood flow and sweating. The influence of estradiol is to promote vasodilation, which, in the skin, results in greater heat dissipation. In the context of blood pressure regulation, both central and peripheral hormonal influences are important as well. Peripherally, the vasodilator influence of estradiol contributes to the lower blood pressures and smaller risk of hypertension seen in young women compared to young men. This is in part due to a mechanism by which estradiol augments beta-adrenergic receptor mediated vasodilation, offsetting alpha-adrenergic vasoconstriction, and resulting in a weak relationship between muscle sympathetic nerve activity and total peripheral resistance, and between muscle sympathetic nerve activity and blood pressure. After menopause, with the loss of reproductive hormones, sympathetic nerve activity, peripheral resistance and blood pressure become more strongly related, and sympathetic nerve activity (which increases with age) becomes a more important contributor to the prevailing level of blood pressure. Continuing to increase our understanding of sex hormone influences on body temperature and blood pressure regulation will provide important insight for optimization of individualized health care for future generations of women.

Keywords: Aging Sex differences Sympathetic nerve activity Thermoregulation Women.


Chapter Review

The kidneys are innervated by sympathetic nerves of the autonomic nervous system. Sympathetic nervous activity decreases blood flow to the kidney, making more blood available to other areas of the body during times of stress. The arteriolar myogenic mechanism maintains a steady blood flow by causing arteriolar smooth muscle to contract when blood pressure increases and causing it to relax when blood pressure decreases. Tubuloglomerular feedback involves paracrine signaling at the JGA to cause vasoconstriction or vasodilation to maintain a steady rate of blood flow.


Glossary

myogenic mechanism: mechanism by which smooth muscle responds to stretch by contracting an increase in blood pressure causes vasoconstriction and a decrease in blood pressure causes vasodilation so that blood flow downstream remains steady

tubuloglomerular feedback: feedback mechanism involving the JGA macula densa cells monitor Na + concentration in the terminal portion of the ascending loop of Henle and act to cause vasoconstriction or vasodilation of afferent and efferent arterioles to alter GFR