Hormonal Control of Blood Pressure Flashcards

1
Q

What are rapidly acting control mechanisms of MAP? List some examples:

A

They are typically nervous reflexes and happen in sends to minutes. The baroreceptors, chemoreceptors, and CNS ischemia response.

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2
Q

What are intermediate acting control mechanisms of MAP? List some examples:

A

They are responses that happen in minutes to hours. The Renin-angiotensin vasoconstrictor mechanism, the dress relaxation mechanism, capillary fluid shift mechanism.

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3
Q

What are long-term acting control mechanisms of MAP? List some examples:

A

They happen in hours to days. Volume control by the kidneys, in particular the renin-angiotensin-aldosterone system.

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4
Q

What is the CNS ischemic response? When is it activated?

A

The arterial pressure elevation in response to cerebral ischemia. 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.

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5
Q

Where is most nervous control of arterial pressure achieved? In what reflexes?

A

Arterial baroreceptors, the chemoreceptors, and the low-pressure baroreceptors all located in the peripheral circulation outside the brain.

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6
Q

What are the four major groups of receptors that compensate for the fall in mean arterial pressure after hemorrhage?

A

High-pressure baroreceptor. Low-pressure baroreceptors. Peripheral chemoreceptors. Central chemoreceptors. Together these responses can increase TPR sufficiently to keep MAP near normal with moderate blood loss (10-20%) but CO remains depressed.

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7
Q

How does the High-pressure baroreceptor work?

A

High-pressure baroreceptors decrease their firing rate leading to increased HR, cardiac contractility, and vasoconstriction.

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8
Q

How does the Low-pressure baroreceptor work?

A

They decrease their firing rate in response to decreased circulating volume. This leads to increased SNS-mediated vasoconstriction, especially the renal bed. (They also stimulate ADH release)

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9
Q

How do the peripheral chemoreceptors work?

A

They respond to local hypoxia by increasing the firing rate of chemoreceptor afferents, leading to increased firing of SNS vasoconstrictor fibers and changes in ventilation.

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10
Q

How do the central chemoreceptors work?

A

They respond to brain ischemial (a fall in pH/ acidosis) leading to a powerful SNS output. (the kidney can actually stop producing urine.

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11
Q

Where is angiotensin I converted to angiotensin II?

A

In the lungs by ACE.

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12
Q

How does angiotensin II work in the blood?

A

It 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.

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13
Q

How does angiotensin II act on the kidney?

A

It acts to retain salt and water, and it also causes the adrenal gland to release Aldosterone, which increases salt and water reabsorption by the kidneys. ANG II also promotes release of ADH/ vasopressin from the posterior pituitary gland.

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14
Q

In hemorrhage how can capillaries increase blood volume?

A

Increased fluid reabsorption by the capillaries in response to a decrease in capillary hydrostatic pressure.

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15
Q

What allows a person to increase or decrease salt intake and keep blood pressure constant?

A

The Renin-angiotensin system.

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16
Q

Where is ADH (aka vasopressin) synthesized, stored and released?

A

Synthesized mainly in the supraoptic nuclei of the hypothalamus and is stored and released at the posterior pituitary.

17
Q

When is ADH released?

A

Increased osmolarity of ECF, decreased blood pressure, decreased blood volume, Angiotensin II stimulates it. It ultimately promotes water reabsorption by the kidney.

18
Q

What affect does Atrial natriuretic peptide (ANP) have?

A

It decreases the release of ADH and aldosterone.

19
Q

ADH, Angiotensin II, and endothelin all have what effect on blood vessels?

A

They constrict them

20
Q

Atrial natriuretic peptide (ANP), Nitric oxide, and prostacyclin (PGI2) all have what effect on blood vessels?

A

They dilate them

21
Q

The afferent arterioles in the renal juxtaglomerular apparatus also contain high-pressure barorecepors, what are they important for?

A

They are involved in regulation of renin release, and consequently, regulation of sodium and water balance, important in long-term regulation of blood pressure.

22
Q

What renal effects does anthill natriuretic peptide have on the kidney?

A

IT causes natriuresis and diuresis and also inhibits aldosterone release by the adrenal medulla.