12/2/2014 Medical Physiology Hormonal Control of Blood Pressure Mary Lou Vallano Flashcards Preview

Unit 5 > 12/2/2014 Medical Physiology Hormonal Control of Blood Pressure Mary Lou Vallano > Flashcards

Flashcards in 12/2/2014 Medical Physiology Hormonal Control of Blood Pressure Mary Lou Vallano Deck (38):
1

What are the three rapidly acting control mechanisms to counter a severe drop in BP, such as that caused by hemorrhage?

1. Baroreceptor reflex
2. Chemoreceptor reflex
3. CNS ischemic response

2

What are the intermediate control mechanisms to counter a severe drop in BP, such as that caused by hemorrhage?

1. Renin-angiotensin vasoconstrictor mechanism
2. Stress relaxation mechanism - not as important
3. Capillary fluid-shift mechanism

3

What are the long-term control mechanisms to counter a severe drop in BP, such as that caused by hemorrhage?

Volume control by the kidneys, especially the renin-angiotensin-aldosterone mechanism *note the potentially infinite gain of this mechanism

4

When does the CNS ischemic response become activated?

When the MAP drops to below about 60 mm HG (very emergency situation)

5

What is the Cushing reaction?

When the CSF pressure = MAP, brain is expanding and blood supply becomes blocked off --> special ischemic response to raise arterial pressure in the brain to higher than CSF to get blood to flow again.

6

T/F: Baroreceptors compensate for the drop in blood volume caused by hemorrhage.

False. Baroreceptoprs and chemoreceptors are technically only concerned with the pressure side of things, even though they may be activated by the same event (hemorrhage). Volume loss is compensated for by thirst, transcapillary refill and renal conservation of salt and water.

7

During hemorrhage, high pressure baroreceptors ___ their firing rate leading to increased HR, cardiac contractility and vasoconstriction.

Decrease

8

During hemorrhage, ______ decrease their firing rate in response to decreased circulating volume. This leads to SNS-mediated vasoconstriction, especially in the renal bed, and stimulate ADH release.

low pressure baroreceptors

9

During hemorrhage, peripheral chemoreceptors respond to what local condition by increasing the firing rate or chemoreceptor afferents, leading to increased firing of SNS vasoconstrictor fibers and changes in ventilation.

Local hypoxia

10

During hemorrhage, central chemoreceptors respond to bran ischemia, characterized by _____, leading to a powerful SNS output, so much so that kidney may stop producing urine.

a drop in pH, aka acidosis

11

In the response to hemorrhage, TPR can be raised to normal with moderate blood loss, but what function remains depressed?

Cardiac output

12

Blood loss triggers what four main receptors to respond?

1. High pressure baroreceptors
2. Low pressure baroreceptors
3. Peripheral chemoreceptors
4. Central chemoreceptors

13

All of these receptor functions are integrated where?
1. High pressure baroreceptors
2. Low pressure baroreceptors
3. Peripheral chemoreceptors
4. Central chemoreceptors

Medullary cardiovascular control center

14

What is the half life of renin?

About 30 min

15

How do we get from renin to increased arterial pressure?

Decreased MAP --> Renin released by kidneys --> Renin cleaves angiotensinogen to Angiotensin I --> Angiotensin I travels to lungs --> Angiotensin I is converted to Angiotensin II by ACE --> Angiotensin II has many functions:
1. ANG II is a potent vasoconstrictor
2. ANG II decreases salt and water excretion from kidneys
3. ANG II causes aldosterone to be released by adrenal gland
4. ANG II stimulates ADH (vasopressin) release from posterior pituitary

16

What inactivates angiotensin II?

Angiotensinase

17

Is Angiotensin II a short or long-acting arterial vasoconstrictor?

Short-acting

18

What is the effect of aldosterone?

Water and salt reabsorption by kidneys

19

T/F: Without the renin-angiotensin response, recovery from blood loss is much more difficult.

True. RAS can pull MAP from 50 to 83 mm HG, but without it, the rise is only 53 to 60 mm HG, which is still very dangerous.

20

Activity of renal sympathetic nerves leads to what two effects?

1. Constriction of renal arterioles
2. Increased renin secretion

21

Fill in the following flow chart with "increase" or "decrease:"
Hemorrhage --> Baroreceptor reflex --> _____ sympathetic outflow --> 1. ___ HR, ___ contractility, ___ CO; ____ 2. constriction of arterioles, ___ TPR, 3. constriction of veins, ___ unstressed volume

All "increase" except for decrease unstressed volume, which means that the veins are kept at a low pressure.

22

What can capillaries do to combat blood loss?

They can increase their fluid reabsorption (in response to a decrease in capillary hydrostatic pressure) which will increase blood volume.

23

Increased salt intake leads to what kind of activity of the renin-angiotensin system?

Decrease

24

What stimulates ADH secretion?

1. ANG II
2. Increased blood fluid osmolality
3. Decreased blood volume
4. Decreased blood pressure
5. Nausea and vomiting

25

What inhibits ADH secretion?

1. Decreased blood fluid osmolality
2. Increased blood volume
3. Increased blood pressure
4. Atrial natriuretic peptide
5. Ethanol

26

How does ADH act on the kidney?

ADH makes the distal convoluted tubules more permeable to water, so actively reabsorbed salt can take the water with it.

27

ADH is synthesized mainly where?

Supraoptic nuclei of the hypothalamus (released by posterior pituitary)

28

How does ADH act on the blood vasculature?

It is a vasoconstrictor

29

ANP decreases the release of what two hormones?

1. ADH
2. Aldosterone

30

In diabetes insipidus, what hormone is not being either made or sensed in the body?

ADH

31

How does ANP act on smooth muscle?

It is a smooth muscle dilator.

32

The endothelium plays an important role in regulating vascular tone by its release of __1__ and __2__ in response to many factors, including shear stress, acetylcholine and bradykinin.

1. NO
2. PGI2 (prostacyclin)

33

The endothelial cell surface (especially in the lungs) has what important enzyme?

ACE

34

In ANG I a totally inactive compound?

Mostly. ANG I has a mild vasoconstrictor effect, but it's nothing compared to ANG II.

35

Afferent arterioles in the renal juxtaglomerular apparatus (kidney) are considered what type of baroreceptor?

High pressure

36

Where are low pressure baroreceptors found?

Pulmonary and cardiac circulation

37

ANP is released by:

Cardiac atria

38

The renal effects of increased blood volume are:

1. Diuresis
2. Natriuresis

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