Specific classes of antihypertensive drugs

If you know these mechanisms, its easy to understand how drugs counteract HTN.

1. Diuretics (thiazides are most commonly used). They act in the kidney and eliminate sodium and water, leading to lower blood volume and lower BP. Thiazide may also have an effect on K+ channel activation and stabilization of membrane potentials. An unwanted effect of thiazides is loss of potassium.

2. Beta-adrenergic receptor blockers (propranolol). These drugs reduce cardiac output and may have more general sympatholytic effects.

3. Centrally active sympatholytics (clonidine) excites pre-synaptic adrenergic alpha-2 receptors that have a negative feedback on release of norepinephrine.

4. Peripherally acting sympatholytics: Reserpine (historically important, never used on people anymore) depletes norepinephrine stores by inhibiting amine pumps. Guanethedine (which is seldom prescribed but still available) depletes the release of norepinephrine from nerve terminals. Prazosin blocks alpha-1 receptors, preventing effects of norepinephrine.

“Look up in book:” direct vasodilators like minoxidil (improves potassium channels) or hydralazine (mechanism not known, but directly relaxes smooth muscle, secondary effects= tachycardia). So when you have any drug that will primarily decrease the BP, the baroreceptors will be excited… this is a complex system and if you screw with one thing, there will be repercussions.

Category: Pharmacology Notes