Pharmacodynamics
o Inhibition of ACE activity results in decreased production of both angiotensin II and
aldosterone:
Decreased vasomotor tone
Smooth muscle relaxation
Decreased aldosterone -> decreased Na/H 2O retention -> decreased bld volume
Decreased BP
o Facilitates the breakdown of bradykinin into inactive fragments, reducing action ->
decreased extravascular smooth muscle relaxation.
o Reno-protective for individuals with proteinuria but is not as protective in renal patients
without proteinuria.
Pharmacotherapeutics
o CONTRAINDICATIONS:
Bilateral renal artery stenosis- vasodilating effect of this drug causes
inadequate perfusion that can lead to ischemic renal failure
Angioedema
Pregnancy
Hyperkalemia
o CAUTIOUS USE:
Impaired renal function
Older adults
Hypovolemic/hyponatremic states
Hepatic impairment
Clinical Use
o Hypertension
o Hypertensive proteinuric diabetes- to prevent diabetic nephropathy
o Angina and Ischemic heart disease (ACEI recommended for all symptomatic patients
with chronic stable angina to prevent MI or death and to reduce symptoms)
o Post MI
o Heart Failure (ACEIs are a cornerstone of HF therapy, and are recommended for patients
with hx of DM, atherosclerotic vascular disease, or HTN)
Drug Interactions
o Cimetidine: increases levels of free drug
o Additive hypotensive effects: diuretics, nitrates, phenothiazines, acute ETOH ingestion
o Hyperkalemia: potassium supplements, potassium-sparing diuretics, cyclosporine
o Increased lithium levels and symptoms of toxicity
o NSAIDS: reduced antihypertensive effects
, Adverse Drug Reactions
o Angioedema (related to increased bradykinin association with inhibition of ACE): 3- to -
4- fold higher risk among African Americans
o Cough – common (common reason of discontinuance of the drug); common among
white population
Dry, hacking
Usually occurs in the first week of therapy
o Hypotension
o Headache
o Fatigue
o Orthostatic hypotension
o Less common: rash (captopril), neutropenia (high doses), renal impairment,
concomitant collagen diseases
o Photosensitivity (enalapril, quinapril, ramipril)
Pharmacodynamics
o Blocks the AT II receptor that leads to:
CNS- decreased vasopressin -> vasodilation
Decreased aldosterone -> decreased Na/H 2O retention -> decreased bld volume
Smooth muscle relaxation
Decreased BP
Pharmacotherapeutics
o CONTRAINDICATIONS:
Bilateral renal artery stenosis- vasodilating effect of this drug causes
inadequate perfusion that can lead to ischemic renal failure
Angioedema
Pregnancy
Hyperkalemia
o CAUTIOUS USE:
Impaired renal function
Older adults
Hypovolemic/hyponatremic states
Hepatic impairment
Clinical Use
o Hypertension
o Hypertensive proteinuric diabetes- to prevent diabetic nephropathy
o Post MI
Drug Interactions
, o CYP450 A34 and 2C9 lowers the levels of losartan and irebesartan.
o Cimetidine: increases levels of free drug
o Additive hypotensive effects: diuretics, nitrates, phenothiazines, acute ETOH ingestion
o Hyperkalemia: potassium supplements, potassium-sparing diuretics, cyclosporine
o Antacids: increases digoxin or lithium toxicity; decreased absorption of ACEI
o NSAIDS: reduced antihypertensive effects
Adverse Drug Reactions
o Hypotension
o Headache
o Fatigue
o Orthostatic hypotension
o Photosensitivity (valsartan)
CALCIUM CHANNEL BLOCKERS (CCB)
Dihydropyridines
o “- pine”
o Amlodipine (not recommended for children <6yo), felodipine, nifedipine, isradepine,
nicardipine
Type 1 CCB
o Diltiazem, verapamil (also Class IV antiarrhythmic drugs)
FIRST LINE for African Americans with HTN (also thiazide-type diurectics)
Pharmacodynamics
o Directly block the Ca++ influx -> decreased transmembrane Ca++ content -> prolonged
vascular smooth muscle relaxation
o Relaxes arterial smooth muscles (but have little effect on venous beds) -> reduced
afterload (but limited effect on cardiac preload)
o Reduces cardiac muscle contractility (negative inotropism) and decreases SA and AV
nodal conduction velocity.
Nifedipine (Adalat, Procardia): do not affect the rate of Ca++ channel recovery
on nodal conduction (no effect on AV conduction)
Verapamil (Calan, Isoptin): affects openings of Ca++ channels, also decreases the
rate of recovery -> depression of SA node firing and slowing AV nodal
conduction
Pharmacotherapeutics
o CONTRAINIDCATIONS:
Verapamil: has the strongest negative inotropic effect and SHOULD BE AVOIDED
in HF, bradycardia, and AV block.
Type 1 CCB: early post MI, ventricular dysfunction, SA or AV nodal conduction
disturbances, SBPs <90
Dihydropyridines: significant peripheral edema, unstable angina
o CAUTIOUS USE:
Severe hepatic impairment
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