1) Antihypertensive Drugs:
➢ ACE Inhibitors
➢ Angiotensin II-Receptor Antagonists
➢ Renin Inhibitors
➢ Calcium Channel Blockers
2) Antianginal Drugs
➢ Organic Nitrates
➢ Calcium Channel Blockers
3) Drug Treatment of Heart Failure
➢ Renin-Angiotensin System Blockers
➢ Direct Vasodilators
➢ Inotropic Agents
➢ Aldosterone Antagonists
4) Drug Treatment of Cardiac arrhythmias
➢ Class I (Sodium Channel Blockers)
➢ Class II ((-adrenoreceptor Blockers)
➢ Class III (Potassium Channel Blockers)
➢ Class IV (Calcium Channel Blockers)
Hydrochlorothiazide is a thiazide diuretic. The thiazide derivatives act mainly in the distal tubule to decrease the reabsorption of sodium by inhibition of a Sodium/Chloride co-transporter on the luminal membrane of the distal convulated tubule. These drugs increase the concentration of sodium and chloride in the tubular fluid. Bumetanide and Furosemide are loop diuretics. They inhibit the co-transport of sodium/potassium/2 chloride ions in the luminal membrane in the ascending limb of the loop of Henle. Therefore, the reabsorption of these ions is decreased. Eplerenone, Spironolactone and Triamterene are potassium-sparing diuretics. Spironolactone antagonizes aldosterone at intra-cellular cytoplasmic receptor sites. The spironolactone-receptor complex is inactive. That is, it prevents translocation of the receptor complex into the nucleus of the target cell. Thus, it can not bind to DNA. This results in a failure to produce proteins that are normally synthesized in response to aldosterone. These mediator proteins normally stimulate the sodium/potassium exchange site of collecting tubule. Thus, a lack of mediator protein prevents sodium reabsorption and, therefore, potassium and hydrogen ion secretion. Triamterene and amiloride block Na-ion transport channels resulting in a decrease in Na/K exchange. Although, they have a K-sparing diuretic action similar to that of spironolactone, their ability to block the Na/K exchange site in collecting tubule does not depend on the presence of aldosterone.
The (-Blockers reduce blood pressure primarily by decreasing cardiac output. They may also decrease sympathetic out-flow from CNS and inhibit the release of renin from the kidneys. Thus decreasing the formation of angiotensin II and the secretion of aldosterone. The prototype (-Blockers is propranolol, which acts at both (1 and (2 receptors. Selective blockers of (1 receptor, such as metoprolol and atelolol, are among the most commonly prescribed (-Blockers.
The ACE inhibitors lower blood pressure by reducing peripheral vascular resistance without reflexively increasing cardiac output, rate, or contractility. These drugs block the ACE that cleaves the angiotensin I to form the potent vasoconstrictor angiotensin II. The converting enzyme is also responsible for the breakdown of...