ACEIs and ARBs Flashcards
ACEIs
captopril
enalapril
enalaprilat
-pril
ARBs
Losartan
Valsartan
-tan
drugs that block renin secretion
clonidine
propranolol
renin inhibitors
aliskriren
AT1R
Gq -> PLC -> IP3 &DAG -> SM contraction
AT2R
bradykinin and NO production
ACEIs
lowers BP by decreasing TPR
CO and HR not changed, making these agents an excellent choice in athletes
ACEIs indications
HTN, nephropathy, HF, left ventricular dysfunction, AMI, prophylaxis of CVD events
ACEI adverse effects
hypotension acute renal failure hyperkalemia dry cough (common reason for termination) angioedema
ACEI and pregnancy
Contraindicated
First semester- teratogen
Second and third trimester- fetal hypotension, anuria, renal failure, death
ACEI Drug interactions
should avoid K supplements and K sparing diuretics and nonsteroidal anti-inflammaotry drugs
ARB MOA
block AT1R
no effect on bradykinin metabolism therefore more selective antagonits of angiotensin effects than ACE inhibitors
ARB indications
used to treat HTN, diabetic nephropathy, HF, or left ventricular dysfunction after AMI, prophylaxis of CV events
Differences btwn ARBs and ACEIs
ARBs reduce activation of AT1R more effectively then ACEIs
ARBs permit activation of AT2Rs
ACEIs increase the levels of a number of ACE substrates including bradykinin
ARB adverse effects
similar to ACEIs, but cough and angioedema less common
ARB contraindications
pregnancy
nondiabetic renal disease
K supplements and K sparring diuretics
clonidine MOA
agonist of alpha 2 receptors in brain-> inhibition of sympathetic vasomotor centers -> centrally mediated reduction in renal sympathetic n activity -> reduction of renin
propranolol MOA
non-specific antagonists of beta R
act on JG cells by blocking beta1R stimulated release of renin and thereby decrease bp
also decreases BP by decreasing CO and decreasing sympathetic outflow from the CNS
aliskiren
PO for HTN
dose-dependent reduction in plasma renin activity
does not cause a rise in plasma renin activity in contrast to ACEIs, ARBs, and diuretics
decreased BP
contraindicated in pregnancy and renal insufficiency
PRC
increased by: direct renin inhibitors, ACEIs, ARBs, diuretics
no change w/CCBs
decreased w/beta blockers
PRA
increased by ACEIs, ARBs, and diuretics
no change w/CCBs
decreased w/direct renin inhibitors and beta blockers
ANG I
increased w/ACEIs, ARBs, diuretics,
no change w/CCBS
decreased w/ direct renin inhibitors, and beta blockers
ANG II
increased w/ARBs and diuretics
non change w/CCBs
decreased w/direct renin inhibitors, ACEIs, and beta blockers
ACE
no change w/direct renin inhibitors and ARBs
decreased w/ACEIs
Bradykinin
no change w/direct renin inhibitors and ARBs
increased w/ACEIs
AT1R
inhibited by ARBs
AT2R
stimulated by ARBs