Lecture 18: CVS Regulation II

Question 1

Baroreceptors

Answer 1

Arterial receptors in carotid sinus + aortic arch that are highly sensitive to stretch; innervate afferent neurons to the brain stem -> CVCCs. Rate of discharge directly proportional to MAP
Primary short-term regulator of BP

Question 2

Medullary CV center (medulla oblongata)

Answer 2

Primary integrating center for baroreceptor reflexes; determines AP freq. from CV center to vagal + symp. neurons

Question 3

Baroreceptor control of hormones

Answer 3

Baroreceptors also control angiotensin II generation, vasopressin secretion

Question 4

Arterial Baroreceptor Reflex

Answer 4

Decreased baroreceptor AP freq induces:
-Increased HR (more symp., less parasymp.)
-Increased ventr. contractility (more symp.)
-Increased arteriole constriction (symp., angio-II, ADH)
-Increased venous constriction (symp.)

Question 5

Baroreceptor adaptation

Answer 5

Increased arterial P above set point for several days will result in chronic hypertension as baroreceptors adjust their set point higher

Question 6

Other baroreceptors besides cardiac sinus, aortic arch

Answer 6

Large systemic veins, pulmonary vessels, heart walls - mediate feedforward reflexes in addition to the usual ones

Question 7

Long term BP regulation mechanism

Answer 7

Blood volume: regulated through Na+/H2O excretion/reabsorption in negative feedback loops via the kidneys

Question 8

Cushing’s phenomenon

Answer 8

Acute elevated ICP leads to a profound increase in MAP.

Question 9

Baroreceptor firing

Answer 9

Increasing pressure -> actively increasing AP freq.
Dropping pressure -> quiescent firing

Changes are not symmetrical!

Question 10

RAAS process

Answer 10

1. Low BP triggers JGA to release renin
2. Renin cleaves circulating angiotensinogen (liver secreted) to angiotensin I in veins
3. Angiotensin I interacts w/ Angioten. Converting Enzyme on endothelial cells
4. ACE converts A1 to A2

Question 11

Effects of angiotensin II

Answer 11

1. Vasoconstrict arterioles
2. Facilitate NE release from neurons
3. Stimulate pressor area in brain
4. Trigger aldosterone release -> Na+ retention in all fluid secreting surfaces
5. Stimulate thirst - behavioral change
6. Stimulate ADH release for H2O retention

Question 12

ADH release and effects

Answer 12

ADH synth/secreted from post. pituitary. Can be stim. by osmoreceptors in brain. High ADH causes vasoconstriction everywhere except brain and heart (dilation through NO release from arterioles)

Question 13

Atrial Natriuretic Peptide

Answer 13

ANP produced by atria, opposes effects of A2

Question 14

ANP effects

Answer 14

1. Block ACh release from PreGSNs
2. Inhibit α-1 receptor synthesis
3. Inhibit renin synthesis
4. Inhibit pressor area
5. Inhibit aldosterone secretion
6. Inhibit renal Na+ retention
7. May inhibit ADH secretion

Question 15

Epinephrine secretion

Answer 15

PreGSNs stimulate adrenal medulla to secrete epinephrine

Question 16

Epinephrine effects

Answer 16

β-1 binding (heart): increase HR, contractility
α-1 binding (veins): increase venous tone
β-2 binding (arterioles): vasodilation
α-1 binding (arterioles): vasoconstriction

Question 17

Adrenergic receptor balance on arterioles

Answer 17

Arterioles have α-1 and β-2 doing opposing things (constrict./dilate); β-2 has higher affinity so dominates @ low epi. High epi -> α-1 overpowers

Question 18

Fight or flight

Answer 18

Higher center coordination selectively increases pressor response for heart, veins, arterioles.
For heart, brain, sk. muscle arterioles -> vasodilation.
NTS inhibition -> ignores baroreceptor reflex signals

Question 19

Fight or flight sk. muscle innervation mechanism

Answer 19

Sk. muscle dilation via:
1. Selective withdrawal of sympathetic tone
2. Epi binding to β-2