Hormonal Control of Blood Pressure Flashcards

1
Q

what are the two main goals when there is severe hemorrhage?

A

respond rapidly to perfuse vital organs and gradually replenish blood volume

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2
Q

what are the rapid acting control mechanisms in response to acute change in blood pressure? what types of responses are these?

A

baroreceptors, chemoreceptors and CNS ischemic response.

these are nervous reflexes

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3
Q

what are the three intermediate controls of blood pressure?

A

renin-angiotensin vasoconstrictor mechanism, capillary fluid shift mechanism and the stress relaxation mechanism

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4
Q

what is the long term control of blood pressure?

A

volume control by the kindney, especially the renin-angiotensin-aldosterone system

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5
Q

what occurs when blood flow to the vasomotor center in the brain stem becomes decreased enough to cause cerebral ischemia?

A

the vasoconstrictor and cardioaccelerator neurons in that area become strongly excited and blood pressure compensates as much as it possibly can (up to 250 mmHg)

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6
Q

what is the specific cause of the CNS ischemic response?

A

buildup of local concentration of CO2 stimulates vasomotor control centers

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7
Q

what happens to urine production during the CNS ischemic response and why?

A

it slows dramatically and may even stop. this is because the vasoconstriction can be so great that some peripheral vessels become occluded

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8
Q

how far must the arterial pressure fall before the CNS ischemic response occurs? when it is optimal?

A

must be down to 60 mmHg but is optimal at 15-20 mmHg

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9
Q

what does the Cushing reaction respond to?

A

increased pressure of cerebrospinal fluid around the brain that cuts off blood flow to the brain

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10
Q

how does the cushing reaction respond to ischemia?

A

it initiates the CNS ischemic response so that the arterial pressure rises to a pressure above the intracranial pressure so there is blood flow

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11
Q

what are the four major groups of receptors that compensate for a large fall in mean arterial pressure?

A

high and low pressure baroreceptors, peripheral chemoreceptors and central chemoreceptors

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12
Q

what response do high pressure baroreceptors have to decreased pressure and what is the result?

A

decreased firing rate

increases heart rate, cardiac contractility and vasoconstriction

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13
Q

what do low pressure baroreceptors respond to and what does it mediate?

A

decrease firing rate responding to decreased circulating volume leads to SNS mediated vasoconstriction and ADH release

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14
Q

what do peripheral chemoreceptors respond to and what do they cause?

A

respond to hypoxia by increasing firing rate and increases vasoconstriction and changes ventilation

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15
Q

where can central chemoreceptors be found and what do they respond to? what effect does this have?

A

respond to brain ischemia (acidosis) and mediate the CNS ischemic response

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16
Q

the major compensations that are mediated with blood loss can keep MAP normal with what amounts of blood loss?

A

15-20% blood loss

17
Q

where is renin secreted and what is its effect?

A

secreted by the kidneys and it cleaves the circulating protein angiotensinogen to angiotensin I

18
Q

where is angiotensin I converted to angiotensin II and by what enzyme?

A

in the lungs by angiotensin converting enzyme (ACE)

19
Q

what is the vascular effect of angiotensin II?

A

it is a powerful short acting arterial vasoconsrictor and causes venoconstriction to increase venous return as well

20
Q

what effect does angiotensin II have on the kidney, brain and adrenal gland?

A

kidney- retains salt and water
brain-promotes release of ADH
adrenal gland- causes the release of aldosterone

21
Q

what is the effect of aldosterone?

A

increases the salt and water reabsorption by the kidneys

22
Q

what inactivates angiotensin II?

A

angiotensinases

23
Q

how much does the renin-angiotensin vasoconstrictor response return mean arterial pressure after a drop from 100-50 mmHg?

A

can raise pressure back to about 83 mmHg (only raised to 60 mmHg without the response)

24
Q

describe the capillary fluid shift mechanism of responding to a decrease in MAP.

A

decreased intravascular hydrostatic pressure increases fluid resorption in the capillaries and therefore increases blood volume

25
Q

what is unstressed blood volume? what is stressed volume?

A

the volume of blood in the peripheral venous compartment

stressed- the volume in the arteries that produces pressure by stretching the vessels

26
Q

what is the every day function of the renin angiotensin system?

A

allows a person to eat salt in varying amounts without causing great changes in extracellular fluid volume or arterial pressure

27
Q

when salt intake is increased, how does the blood volume and pressure react? what does this do to renin and angiotensin?

A

increased extracellular volume and arterial pressure

decreases renin and angiotensin

28
Q

what is the result of decreased renin and angiotensin on the kidney?

A

decreases retention of salt and water

29
Q

where is antidiuretic hormone manufactured and secreted?

A

synthesized in the supraoptic nuclei of the hypothalamus and is stored and released at the posterior pituitary

30
Q

when is ADH secreted?

A

in response to increased osmolarity of extracellular fluid, decreased volume (low pressure baroreceptors), decreased blood pressure, antiotensin II, and stress

31
Q

what are the major and minor effects of ADH?

A

increase water resorption in the kidney and minor vasoconstrictor effect

32
Q

what inhibits the secretion of ADH?

A

increased blood volume and pressure, ethanol, decreased fluid osmolarity and atrial natriuretic hormone

33
Q

what hormones are smooth muscle dilators and constrictors?

A

dilaor- atrial natriuretic peptide

constriction- ADH and angiotensin II (ACE found on endothelium)

34
Q

other than the carotid sinus and the aortic arch, where are there other high pressure baroreceptors? what do they regulate?

A

in the afferent arterioles in the renal juxtalomerular apparatus. regulate renin release

35
Q

when is atrial natriuretic peptide released and where?

A

when there is volume overload in the atria of the heart