Hormonal Control of Blood Pressure Flashcards
List the 3 rapid mechanisms of arterial pressure regulation.
Rapidly acting control mechanisms are typically nervous reflexes:
1) baroreceptors
2) chemoreceptors
3) CNS ischemic response.
List the 3 intermediate mechanisms of arterial pressure regulation.
Intermediate controls include:
1) renin-angiotensin vasoconstrictor mechanism
2) stress relaxation mechanism (e.g., increased pressure for min-hrs leads to continuous stretch of the vessel to relieve the pressure)
3) capillary fluid shift mechanism (e.g., if capillary pressure falls too low, fluid is absorbed from the tissues through the capillary membranes thus building up blood volume and pressure)
NOTE: during this time, nervous mechanisms become gradually less effective.
List the one long-term mechanism of arterial pressure regulation.
1) Long-term control involves volume control by the kidneys, in particular the renin- angiotensin-aldosterone system.
Briefly analyze figure on pg. 82 & note the rapid, intermediate, and long-term mechanisms of arterial pressure regulation & their relative strengths.
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List the relative timeframes for each of the major arterial pressure regulation systems.
Short tem = seconds
Intermediate = minutes
Long term = Days
Describe the Cushing reflex or response
Cushing reflex or Cushing response is a physiological nervous system response to increased intracranial pressure that results in Cushing’s triad of:
increased blood pressure:
irregular breathing
reduction of the heart rate
It is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation.
Descibe the CNS Ischemic Response
Most nervous control of blood pressure is achieved by reflexes that originate in the baroreceptors, the chemoreceptors, and the low-pressure receptors, all of which are located in the peripheral circulation outside the brain. However, when blood flow to the vasomotor center in the lower brain stem becomes decreased severely enough to cause nutritional deficiency—that is, to cause cerebral ischemia—the vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond directly to the ischemia and become strongly excited. When this occurs, the systemic arterial pressure often rises** to a level as high as the heart can possibly pump. This effect is believed to be caused by failure of the slowly flowing blood to carry carbon dioxide away from the brain stem vasomotor center: At low levels of blood flow to the vasomotor center, the local concentration of carbon dioxide increases (pH decreases) greatly and has an extremely potent effect in stimulating the sympathetic vasomotor nervous control areas in the brain’s medulla.
It is possible that other factors, such as buildup of lactic acid and other acidic substances in the vasomotor center, also contribute to the marked stimulation and elevation in arterial pressure. This arterial pressure elevation in response to cerebral ischemia is known as the central nervous system (CNS) ischemic response.
The ischemic effect on vasomotor activity can elevate the mean arterial pressure dramatically, sometimes to as high as 250 mm Hg for as long as 10 minutes. The degree of sympathetic vasoconstriction caused by intense cerebral ischemia is often so great that some of the peripheral vessels become totally or almost totally occluded. The kidneys, for instance, often entirely cease their production of urine because of renal arteriolar constriction in response to the sympathetic discharge. Therefore, the CNS ischemic response is one of the most powerful of all the activators of the sympathetic vasoconstrictor system.
Despite the powerful nature of the CNS ischemic response, it does not become significant until the arterial pressure falls far below normal, down to 60 mm Hg and below, reaching its greatest degree of stimulation at a pressure of 15 to 20 mm Hg. Therefore, it is not one of the normal mechanisms for regulating arterial pressure. Instead, it operates principally as an emergency pressure control system that acts rapidly and very powerfully to prevent further decrease in arterial pressure whenever blood flow to the brain decreases dangerously close to the lethal level. It is sometimes called the “last ditch stand” pressure control mechanism.
Long-term control involves volume control by the kidneys, in particular the renin- angiotensin-aldosterone system has ______ gain.
infinite
The enzyme ______ is released by the ______ when MAP _____. It persists in the circulation for ____.
Renin cleaves a circulating protein ______ to form ______1. This protein is a weak _______.
ANG I is further converted to ______2, primarily in the lungs by an enzyme in the endothelium of the lung vessels called __________.
ANG II is a powerful but relatively short-acting arterial _______. It _____ MAP by ______ TPR, and also promotes venous return to the heart to some extent by causing _______.
ANG II is important for long-term control of MAP because it _______ renal excretion of salt and water, slowly ______ extracellular fluid volume and, in turn, arterial pressure.
ANG II acts directly on the ______ to retain salt and water, and it also causes the adrenal gland to release ________, which increases salt and water _______ by the ______ which increases blood _____. ANG II also promotes release of ADH/vasopressin from the posterior pituitary gland. Furthermore, ANG II can DIRECTLY increase sodium & water ______ by the kidney (without ALDOSTERONE) via different mechanisms.
ANG II is inactivated by __________.
The enzyme RENIN is released by the kidneys when MAP falls. It persists in the circulation for 30-60 min.
Renin cleaves a circulating protein ANGIOTENSINOGEN to form ANGIOTENSIN I. ANG I is a weak vasoconstrictor.
ANG I is further converted to ANGIOTENSIN II (ANG II), primarily in the lungs by an enzyme in the endothelium of the lung vessels called ANGIOTENSIN CONVERTING ENZYME or ACE.
ANG II is a powerful but relatively short-acting arterial vasoconstrictor. It raises MAP by increasing TPR, and also promotes venous return to the heart to some extent by causing venoconstriction.
ANG II is important for long-term control of MAP because it decreases renal excretion of salt and water, slowly increasing extracellular fluid volume and, in turn, arterial pressure.
ANG II acts directly on the kidney to retain salt and water, and it also causes the adrenal gland to release ALDOSTERONE, which increases salt and water reabsorption by the kidneys (salt reabsorption pulls water) which increases blood volume. ANG II also promotes release of ADH/vasopressin from the posterior pituitary gland (not shown). Furthermore, ANG II can DIRECTLY increase sodium & water reabsorption by the kidney (without ALDOSTERONE) via different mechanisms.
ANG II is inactivated by ANGIOTENSINASES.
Fill in the blanks on the Angiotensen 2 sheet & compare w pg. 85
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What would occur to a patient with and without the renin-angiotensin system during a hemmoarage?
See pg. 86
After acute hemorrhage, enough to cause a drop in arterial pressure from 100 mm Hg to 50 mm Hg, the renin-angiotensin vasoconstrictor response is powerful enough to return pressure back to ~83 mm Hg (more than halfway, solid line) after several minutes. This response can be life-saving, especially in circulatory shock.
In the presence of a renin-blocking antibody (dashed line), recovery was much weaker, returning to 60 mm Hg.
High-pressure baroreceptors ______ their firing rate (___ AP’s) due to _____ in stretch, leading to increased HR, cardiac contractility, and vasoconstriction.
Low-pressure baroreceptors ______ their firing rate in response to decreased circulating _____. This leads to increased SNS-mediated vasoconstriction, especially the renal bed. (They also stimulate ADH release). The low-pressure baroreceptors, are found in ______, in _______, and in the _____ of the heart (the atrial volume receptors).
Peripheral chemoreceptors respond to local hypoxia by ______ the firing rate of chemoreceptor afferents, leading to ______ firing of SNS vasoconstrictor fibers and changes in ventilation.
Central chemoreceptors respond to brain ______ leading to a powerful SNS output (the kidney can actually stop producing urine).
High-pressure baroreceptors decrease their firing rate (___ less AP’s) due to decrease in stretch, leading to increased HR, cardiac contractility, and vasoconstriction.
Low-pressure baroreceptors decrease their firing rate in response to decreased circulating central (venous) volume*. This leads to increased SNS-mediated vasoconstriction, especially the renal bed. (They also stimulate ADH release). The low-pressure baroreceptors, are found in large systemic veins, in pulmonary vessels, and in the walls of the right atrium and ventricles of the heart (the atrial volume receptors).
Peripheral chemoreceptors respond to local hypoxia by increasing the firing rate of chemoreceptor afferents, leading to increased firing of SNS vasoconstrictor fibers and changes in ventilation.
Central chemoreceptors respond to brain ischemia (a fall in pH/acidosis) leading to a powerful SNS output (the kidney can actually stop producing urine).
Review figure pg. 84
Response to hemorrhage involves contributions of the baroreceptors, the renin- angiotensin-aldosterone system, as well as increased ______ by the capillaries in response to a decrease in capillary hydrostatic pressure. Overall, this ______ filtration & ______ reabsorption (more fluid to be absorbed from extracellular compartment).
Response to hemorrhage involves contributions of the baroreceptors, the renin- angiotensin-aldosterone system, as well as increased fluid reabsorption by the capillaries in response to a decrease in capillary hydrostatic pressure. Overall, this decreases filtration & increases reabsorption (more fluid to be absorbed from extracellular compartment).
Review figure pg. 87
When salt intake is increased, there is a ______ in renin-angiotensin release and action. When salt intake is decreased, there is an ______ in renin-angiotensin release and action.
When salt intake is increased, there is a decrease in renin-angiotensin release and action (since ANG II increases salt reabsorption so no need). When salt intake is decreased, there is an increase in renin-angiotensin release and action.
See Review figure pg. 88
Discuss ADH: where it’s made, stored, when it’s released, main functions, when it’s inhibited.
Antidiuretic hormone (ADH; also known as vasopressin ) is synthesized mainly in the hypothalamus and is stored and released at the posterior pituitary.
ADH’s main function is the reabsorption of water.
ADH is released in response to increased osmolarity of extracellular fluid and decreased blood pressure and has the major effect of promoting water reabsorption by the kidney.
ADH is released when you are dehydrated and causes the kidneys to conserve water, thus concentrating the urine and reducing urine volume.
Vasopressin/ADH is also a vasoconstrictor (less strong than its effect on the kidney).
It is released in response to: *increased body fluid osmolality/osmolarity, decreased blood volume (which activates low pressure baroreceptors), and decreased blood pressure.
ADH is inhibited by *decreased body fluid osmolality/osmolarity, increased blood volume, increased blood pressure, alcohol, & ANP (atrial natriuretic peptide–ANP released during increased blood volume) decreases the release of vasopressin/ADH (and aldosterone from the adrenal cortex).
