Lecture 17: CVS Regulation 1

Question 1

Local controls of CV regulation

Answer 1

Mechanisms by which organs/tissues alter their own arteriolar resistance, INDEPENDENT of nerves and hormones

Question 2

Active hyperemia

Answer 2

Refers to an increase in blood flow to a region due to increased metabolic activity; caused by arteriolar dilation

Question 3

Local chemical changes inducing active hyperemia

Answer 3

Low pO2, high pCO2, high H+, high adenosine (ATP use), high K+ (AP firing), high eicosanoids (p-lipid breakdown); increased bradykinin, increased NO (endothelium)

Question 4

Bradykinin

Answer 4

Locally generated peptide, potent vasodilator. Kallikrein cleaves circulating kininogen to bradykinin.

Question 5

Kallikrein

Answer 5

Produced locally with increased metabolic rate, or secreted as prekallikrein by the liver.

Question 6

Flow autoregulation

Answer 6

Maintenance of constant blood flow despite changes in blood pressure

Question 7

Mechanisms of flow autoregulation

Answer 7

1. Metabolic factors just like with active hyperemia
2. Myogenic response

Question 8

Myogenic response

Answer 8

Mechanism of flow autoregulation. Smooth muscle stretch receptors adjust tone accordingly with changes in vessel stretching to maintain a constant blood flow (less stretch -> less tone/contraction, more stretch -> more tone)

Question 9

Reactive hyperemia

Answer 9

Phenomenon of profound transient increases in blood flow after restoring completely occluded blood supply. Extreme form of active hyperemia

Question 10

Extrinsic controls of CV regulation

Answer 10

Aka reflex controls; hormonal + neural innervation

Question 11

ANS innervation of arterioles

Answer 11

Sympathetic only. NE -> α adrenergic receptors -> vasoconstriction; β in heart.
Innervation always occurs at a basal level/tone which is increased or decreased.

Question 12

Purpose of intrinsic controls vs extrinsic controls

Answer 12

Intrinsic controls coordinate local needs, while extrinsic reflex controls are concerned with serving the whole body.

Question 13

ANS non-cholinergic/non-adrenergic innervation of CV

Answer 13

These neurons release other vasodilators e.g. NO, found in places like enteric NS or penis/clitoris (drug targets for viagra/cialis.

Question 14

Hormonal CVS regulation

Answer 14

Epi -> β2 receptors -> dilation, especially in sk. muscle arterioles
Epi -> α receptors -> vasoconstriction
Angiotensin/vasopressin -> vasoconstriction
ANP -> dilation

Question 15

Endothelial paracrine secretions

Answer 15

NO, Prostacyclin, Endothelin-1

Question 16

Endothelial NO secretion

Answer 16

NO is continually secreted at a basal level by endothelial cells and increases rapidly in response to many reflex/local controls

Question 17

Endothelial prostacyclin secretion

Answer 17

aka prostaglandin I2 (PGI2); low basal level but can increase significantly for vasodilation

Question 18

Endothelin-1

Answer 18

ET-1 is a vasoconstrictor that is usually paracrine but can also act as a hormone at high enough concentration

Question 19

Overall CVS regulatory scheme

Answer 19

-Higher centers
-Cardiovascular Control Center (CVCC) in lower pons, medulla)
-Effectors (arterioles, veins, heart)
-Sensors (large arteries, heart)

Question 20

Myogenic response mechanism

Answer 20

Distention induces opening of Ca++ stretch channels, which induces more Ca++ release from sm. muscle SR -> increase of tone w/ stretch

Question 21

Important factors for smooth muscle contractility

Answer 21

1. Intracellular Ca++ levels (influences MLCK activity)
2. K+ conductance
3. Direct inhibition of contractile proteins

Question 22

Cardiovascular Control Center regions

Answer 22

1. Nucleus Tractus Solitarius (NTS)
2. Vagus nerve cell bodies (X, parasymp.)
3. Depressor area (D)
4. Pressor area (P)

Question 23

Depressor and pressor areas of CVCC

Answer 23

Converge on pre-ganglionic sympathetic neurons and influence downstream post-GSN stimulation of effectors via NE. Depressor = inhibitory, pressor = excitatory

Question 24

CVCC regulation of veins

Answer 24

Veins are the primary capacitance vessels; increase in venous pressure (w/ symp. stim.) increases venous return, helping redistribute blood.

Question 25

CVCC regulation of the heart

Answer 25

Parasymp. and symp. are in opposition, e.g. vagal ACh lowers HR, symp. stim. increases HR. Both have tone but vagal dominates at rest. Contractility is primarily controlled by sympathetic tone.