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Ruth Anderson & Robert Stone
Ruth Anderson: Case of secondary hypertension and hypokalemia in a young woman. Be able to recognize clinical characteristics of secondary hypertension and understand underlying physiology to enable diagnostic and treatment strategies
Robert Stone: Understand blood pressure, renin-angiotensin system, and atherosclerosis
Renin-Angiotensin-Aldosterone System
ACEI and pregnancy
Mechanism of action
Monitoring of ACEI
Hypokalemia/hyperkalemia as result of RAAS
Hypertension
Classification of primary and secondary & etiology
DEEPICT secondary HTN
Symptoms, labs, when to admit?
Treatments – Beta-blockers, Ca2+ channel blockers, diuretics
Refractory HTN
Atherosclerosis and HTN
Review of Case
Silver wiring
Creatinine clearance
Calculation & what it means
Explain CHF – relation to OTC medications (NSAIDs)
Renin-Angiotensin System
Renin is serine acid protease protein enzyme released by kidneys when arterial pressure falls too low
Renin synthesized and stored in inactive form (prorenin) in juxtaglomerular cells (JG cells) of kidneys
JG cells are modified smooth muscle cells in walls of afferent arterioles immediately proximal to glomeruli
Decreased arterial pressure intrinsic reactions in kidneys cause many prorenin molecules in JG cells to split and release renin
Most renin enters renal blood and passes out of kidneys into circulation
Small amts of renin remain in local fluids of kidney and initiate intrareneal functions
Renin acts enzymatically on another plasma protein called angiotensinogen to release 10-aa peptide, angiotensin I
Angiotensin I has mild vasoconstrictor properties but not enough to cause significant changes in circulatory function
w/in few seconds to minutes after formation of angiotensin I, 2 more aas are split off from angiotensin I to form 8-aa peptide, angiotensin II
conversion to AII occurs in lungs while blood flows through small vessels of lungs, catalyzed by angiotensin converting enzyme that is present in endothelium of lung vessels
AII is powerful vasoconstrictor, but only persists in blood for 1-2 mins b/c its rapidly inactivated by multiple blood and tissue enzymes collectively called angiotensinases
Angiotensin II has 2 main effects that can elevated arterial pressure
vasoconstriction in many areas of body occurs rapidly – acute effect
arterial vasoconstriction > venous vasoconstriction
arteriole constriction increases total peripheral resistance raises arterial pressure
mild venous constriction promotes increased venous return of blood to heart helps heart pump against increasing pressure
decreased excretion of both salt and water by kidneys – long-term effect
causes increase in extracellular fluid volume increased arterial pressure during subsequent hours and days
renin-angiotensin vasoconstrictor system requires 20 min to become fully active
thus: slower to act for pressure control than nervous reflexes and sympathetic norepinephrine-epinephrine system
angiotensin II causes kidneys to retain both salt and water in 2 major ways:
AII acts directly on kidneys to cause salt and water retention
Mechanisms of AII on kidneys:
Constrict renal arterioles diminishes blood flow through kidneys less fluid filters through glomeruli into tubules
Slows flow of blood through kidney reduces pressure in peritubular capillaries causes rapid reabsorption of fluid from tubules
Direct effect on tubular cells increase tubular reabsorption of sodium and water
AII causes adrenal glands to secrete aldosterone aldosterone increases salt and water reabsorption by kidney tubules
Activation of renin-angiotensin system causes rate of aldosterone secretion to also increase
Function of aldosterone increase sodium reabsorption by kidney tubules increases total body extracellular fluid sodium increased Na causes water retention increases extracellular fluid volume long-term elevation of arterial pressure
Direct effect of angiotensin on kidneys is perhaps 3 or more times as potent as indirect effect acting through aldosterone
Role of Renin-Angiotensin system in maintaining normal arterial pressure despite salt intake
Increased salt intake elevated extracellular fluid volume elevated arterial pressure increased blood flow through kidneys reduced rate of secretion of renin decreased renal retention of salt and water return of extracellular fluid volume almost to normal return of arterial pressure almost to normal
Thus: renin-angiotensin system is automatic feedback mech. that helps maintain arterial pressure at or near normal level even when salt intake is increased
When system functions normally, arterial pressure rises no more