Lecture 26

Question 1

Why modify VSM in heart failure?(2)

Answer 1

reduce preload (partially)
reduce afterload (completely)

Question 2

why modify VSM in hypertension?

Answer 2

prevent consequences (ie retinal detachment)

Question 3

why modify VSM in chronic renal failure?

Answer 3

restore glomerular filtration

Question 4

Factors that affect SV

Answer 4

MAP=COxTPR(TPR is afterload)
CO=HRxSV
SV is contractility and EDV-ESV(ESV is afterload)
EDV is preload and venous return

Question 5

What makes VSM contract?

macro(2) and micro(3) control

Answer 5

Macro-
*Sympathethic NS and RAAS
Micro-
*sheer stress
*pH, lactate, pO2
*endothelin

Question 6

SNS—-

Answer 6

alpha-contraction

beta-relaxation

Question 7

How does VSM contract at alpha receptor(4 steps)

Answer 7

NA binding->IP3 and DAG inc->inc intracelluar Ca->contraction

Question 8

How does VSM relax at beta receptor

Answer 8

NA binding->inc adenyl cyclase->inc cAMP->inactive MLCK->relaxation

Question 9

VOCC found in (3)

Answer 9

VSM
cardiac cells
nerves

Question 10

L-type VO Ca channels found in (2)

Answer 10

VSM

Cardiac muscle-nodal tissue

Question 11

Nitrates
what type of drugs
mechanism of action
used in
what do they do 
bioavailability

Answer 11

venodilator drug
-NO doNOrs
inc NO->cGMP->vasodiation
-used in acute decompensated heart failure
reduce preload
-low bioavailability (1st pass effect)

Question 12

Arteriodilator drugs- hydralazine
mechanism
what does it do(3)
side effects(2)

Answer 12

mechanism unknown
-drop arterial pressure quickly
-reduce afterload
-dec pulmonary edema
side effects- hypotension (always use with diuretic) and reflex tachycardia

Question 13

Ca channel blockers
what type of drug
mechanism of action
which channels are more targeted

Answer 13

arterial dilator
block L type Ca channels (heart and VSM)
bind to receptors in the active state and delay recovery to resting state
bind to Ca channel from the inside
more active channels more targeted(use dependence)

Question 14

Ca channel blockers(arterial dilator) effects on HR

Answer 14

SA pacemaker activity and AV conduction slowed->dec HR

Question 15

Ca channel blockers(arterial dilator) effect on myocardium

Answer 15

dec entry of Ca into the cell-> dec force of contraction

Question 16

Ca channel blockers(arterial dilator) effect on vascular vessels

Answer 16

prevent rise in intracellular Ca needed for the formation of MLCK so ->relaxation(dilation of systemic arteries and arterioles)

Question 17

alpha blockers
what type of drug
mechanism of action
what do they do

Answer 17

indirect vasodilator drug (arterial dilator)

• block alpha receptors on VSM->arterial dilation->dec TPR and BP
• Less NA binding->dec IP3 and DAG->dec intracellular Ca->relaxation

Question 18

Beta blockers
what type of drug
Cardiac effect-
Renal effect-
Side effects-(3)

Answer 18

• indirect vasodilator (arterial dilator)
• dec HR (SA node), dec contractility (SV) therefore dec CO (dec arterial pressure)
• block B1 receptors on JG cells-> dec renin release and dec angiotensin formation (dec preload/blood volume) therefore dec TPR and dec MAP
• cold extremities, fatigue (dec CO), bronchoconstriction (asthma)

Question 19

Chronic activation of RAAS
-persistent vasoconstriction->
inc blood volume ->
inc angiotensin ->

Answer 19

inc preload and afterload
inc preload
dec baroreceptor sensitivity

Question 20

Drugs affecting RAAS (2)

Answer 20

ACE inhibitor

Angiotensin 2 receptor antagonists

Question 21

drugs affecting RAAS- angiotensin 2 receptor antagonists(2)

Answer 21

more selective that ACE inhibitors

more complete inhibition of angiotensin

Question 22

drugs affecting RAAS-ACE inhibitor

Answer 22

• dec vasoconstriction
• inhibit aldosterone release (dec Blood vol)
• reduce afterload (TPR)
• reduce preload (blood volume)
• MUST TEST RENAL FUNCTION FIRST