Lecture 6 (RAAS and Hemodynamics) Flashcards
Function of Renin:
necessary for angiotensin II synthesis
Function of Angiotensin II:
- vasoconstrictor
- stimulates aldosterone secretion from adrenal cortex
Function of Aldosterone:
- promotes Na+ conservation by kidneys; H2O follows Na+
- increases intravascular volume
- vasoconstrictor
All angiotensin II bioactivity in vascular smooth muscle and cardiac muscle is mediated by what receptor?
AT1
Actions of angiotensin II that lead to increased blood pressure (4):
- vasoconstriction
- block in high pressure baroreceptor activity
- increased aldosterone levels
- stimulation of norepi release from post-ganglionic SNS fibers
Angiotensin II can block high pressure baroreceptor input. How does this cause an increase in BP?
- endogenous counter-response to elevated BP is neutralized.
- SNS not shut off in response to elevated BP.
- SNS has free-reign to maintain increased BP.
Where are receptors for RAAS (angiotensin II and aldosterone) located?
- myocardium
- vascular smooth muscle
- kidney
Effect of RAAS (aldosterone and angiotensin II) on the heart:
- contributes to left ventricular hypertrophy
- increased wall stress and oxygen demand
- reduced ejection fraction
Effect of RAAS (aldosterone and angiotensin II) on vascular smooth muscle:
- leads to tunica intima and tunica media thickening
- can cause vascular stenosis
Effect of RAAS (aldosterone and angiotensin II) on the kidney:
- impairs normal renal function
- can lead to renal failure.
Treatments for hypertension:
- ACE inhibitors (angiotensin II)
- ARBs (AT1 receptors)
- Diuretics (aldosterone)
- Calcium channel blockers (amlodipine)
- beta-blockers (SNS)
Function of verapamil and cardizem:
- blocks Type L calcium channels in the heart.
- help reduce heart rate by increasing AV nodal delay.
Function of amlodipine:
- blocks Type L calcium channels in vascular smooth muscle.
- prevents vasoconstriction.
Primary hypertension:
- hypertension due to an unknown cause.
- treatable with general hypertension protocol.
- ACE inhibitors, ARBs, calcium channel blockers, etc.
Secondary hypertension:
- hypertension due to another medical condition.
- not treatable with general hypertension protocol.
How, specifically, does using a beta-blocker decrease blood pressure?
- beta-blockers block SNS effects on the heart.
- decrease HR and inotropy, and therefore CO.
- CO = SV x HR.
- MAP = CO X TPR.
General primary hypertension treatment protocol:
-
First:
- thiazide diuretic
-
Second:
- thiazide diuretic + ACE inhibitor/ARB
-
Third:
- thiazide diuretic + ACE inhibitor/ARB + Ca2+ channel antagonist

The four body systems involved in hypertension, and drugs that target their function:
-
cardiac
- calcium channel blockers, beta-blockers
-
renal
- diuretics, ACE inhibitors, ARBs
-
vascular smooth muscle
- calcium channel blockers, ACE inhibitors, ARBs, alpha-1 receptor blockers
-
ANS
- beta-blockers
Blood vessels with the highest velocity and lowest velocity of flow:
- highest velocity: aorta
- lowest velocity: capillaries
Blood vessels with the highest and lowest total cross-sectional area:
- highest: capillaries
- lowest: aorta
Blood vessels with the highest and lowest transmural (wall) pressure:
- highest: aorta
- lowest: vena cava
Total peripheral resistance equation:
-
TPR = (Pa - Pv)/Qt.
- Qt = cardiac output (CO = SV x HR).
- Pa - Pv = CO x R
60% of total peripheral resistance is due to:
- arteriolar resistance
- Arterioles can undergo 4x changes in lumen diameter, which leads to up to a 256x change in conductance.
Which blood vessel has the greatest influence over total peripheral resistance?
arterioles




