Drug | Mechanism of Action |
ACE inhibitors (captopril, enalapril) | Inhibition of ACE leads to reduced angiotensin II (vasodilation) and aldosterone (reduced Na+ retention) levels and increased bradykinin (--> vasodilation) levels. |
Angiotensin antagonists (losartan and EXP3174) | Inhibition of angiotensin II receptor (--> vasodilation) |
Ca++ antagonists (verapamil, diltiazem) | Block Ca++ channels. Decreased intracellular Ca++ leads to reduced contractility and vasodilatation. |
α1-antagonists (prazosin, doxazocin) | Inhibition of α1-mediated vasoconstriction reduces peripheral resistance and venous pressure. Also improves lipid profile to decrease risk of CAD. |
Sodium nitroprusside | Decomposes to NO, which activate guanylyl cyclase, thus increasing cGMP levels, and causing vasodilatation |
Thiazide diuretics (hydrochlorothiazide, polythiazide) | Reduction of blood volume/indirect vasodilatation |
Centrally acting drugs (clonidine, α-methyldopa) | α2-agonists. False transmitter activates central inhibitory neurons, causing inhibition of NA release and vasodilatation. |
β-antagonists (nonselective - propranolol, selective - atenolol) | Block β1-receptors in heart, causing decreased rate, systolic BP, cardiac contractility, and myocardial O2 demand. Work in heart, kidney (RAS), and CNS |