Intro to Antihypertensive Agents I Flashcards
prehypertension
SBP 120-139
DBP 80-89
recommend lifestyle changes
stage 1 HTN
SBP 140-159
DBP 90-99
begin treating HTN
stage 2 HTN
SBP >160
DBP >100
mean arterial pressure
MAP = CO x TPR
cardiac output
CO = HR x SV
drug strategy with HTN
reduce CO
reduce TPR
compensation for HTN meds**
reflex tachycardia - increased symapthetics
edema - increased renin activity
**so can add different drug to counteract
weight reduction
5-20 decreased SBP
DASH diet
8-14 decreased SBP
dietary sodium reduction
2-8 decreased SBP
physical activity
4-9 decreased SBP
moderation of alcohol
2-4 decreased SBP
antihypertensive sites of action
arterioles
venules
heart
kidneys
major classes of antihypertensive meds
- diuretics
- agents blocking ANG action
- direct vasodilators
- sympathoplegic agents
diuretics
act at kidney tubules
agents that block ANG action
- angiotensin receptors of vessels
- beta-receptors of JG cells
- ACE inhibitors
- renin inhibitors
direct vasodilators
on vascular smooth m.
sympatholytics
- vasomotor center of brain
- beta-receptors of heart
- alpha receptor of vessels
- beta receptors of JG cells
patients with CKD
ACE inhibitors
ARB (angiotensin receptor blocker)
black patients without CKD
thiazide diuretic
calcium channel blockers
nonblack patient without CKD
thiazide diuretic**
ACE inhibitor
ARB
CCB
kidney blood flow
20-25% of CO
carbonic anhydrase
formation/dehydration of carbonic acid in proximal tubule
proximal tubule activity
- active reabsorption of HCO3, NaCl, K, glucose, AAs
- passive reabsorption of water
- Na/K pump maintains Na concentration in cell low
- carbonic anhydrase
**site of action of carbonic anhydrase inhibitors
thin descending loop of henle
water reabsorption
thin ascending loop of henle
impermeable to water, other ions/solutes
thick ascending loop of henle
Na/H/2Cl cotransport
-established concentration gradient
K leak in thick ascending limb
high K in cells - K diffuses back to lumen
-creates positive charge- drives the paracellular reabsorption of Mg, Ca
tubular fluid
concentrated in descending limb and diluted in ascending limb
distal convoluted tubule
- 10% NaCl reabsorbed
- impermeable to water
Na/Cl cotransporter - active NaCl out of lumen
-Ca is reabsorbed by calcium channels
thiazide diuretics
blocks Na/Cl cotransporter in the distal convoluted tubule
Ca reabsorption
distal convoluted tubules
- has Ca channels
- regulated by PTH
-increased PTH/increased reabsorption
most important site of K secretion**
collecting tubule
-site where all diuretic induced K balance changes occur
most diuretics - hypokalemia - bc more sodium to CT lumen > more Na pulled out at ENaC > causes more K secretion
also hypokalemia with metabolic alkalosis > lumen negative favors retention of H+ in lumen > urine pH goes down > body pH goes up
more Na to CT - more K secretion
collecting tubule
- proton pump - increased urine acidity
- ENaC - 2-5% Na reabsorption
creates electrical gradient that facilitates K secretion down concentration gradient
aldosterone
increased ENaC and basolateral Na/K ATPase in collecting tubule
water retention - increase in blood volume and BP
ENaC
in collecting tubule
- increased Na reabsorption
- 2-5% of total
- does create gradient to facilitate K secretion
ADH
aka vasopression
- released from pituitary
- increases aquaporin 2 on collecting tubules
- via V2 receptor
-increased water reabsorption
ADH level control
serum osmolality and volume status
diuretics
- carbonic anhydrase inhibitors
- loop diuretics
- thiazide diuretics
- potassium-sparing diuretics
diuretic use
increase rate of urine flow
edematous and nonedematous states
site of loop diuretics
Na/K/2Cl cotransporter in thick ascending limb
site of thiazide diuretics
Na/Cl cotransporter
site of potassium sparing diuretics
sodium channels
site of potassium sparing diuretics
mineralocorticoid receptors
and sodium channels
