NR 566/ NR566 WEEK 3 Ch. 16, 28, 36, 39, 40 Drugs Affecting the Cardiovascular and Renal Systems. GREAT SUMMARY.
ACEIs (Angiotensin-converting enzyme inhibitors) • Angiotensin II roles in the cardiovascular system: o increases vasomotor tone by direct stimulation of vascular smooth muscle contraction and through the inhibition of endothelial nitric oxide and prostaglandin release, raising BP and decreasing blood flow through arteries, including the coronary arteries. o increases intravascular volume through its stimulation of sodium and water retention (with aldosterone), shifting of the pressure-natriuresis relationship, and altering glomerular hemodynamics. o produced in response to tissue injury. results in stimulation of smooth muscle cell and fibroblast proliferation with thickening of the vessel wall (remodeling). This action, combined with its inhibition of the endothelium's ability to resist monocyte and platelet adhesion, promotes intravascular inflammation and clotting and contributes to the atherosclerotic process. o in the heart causes remodeling, resulting in hypertrophy and fibrosis of myocardial tissue after ischemic injury or in response to persistent afterload. This is a primary mechanism in HF Calcium Channel Blockers (CCBs) • All CCBs relax arterial smooth muscle but have little effect on venous beds. This results in significant reduction in afterload but limited effect on cardiac preload. • Two major classes o Type I – Non-dihydropyridines: affect conduction through the atrioventricular (AV) node and have negative chronotropic effects Diltiazem (Cardizem), verapamil (Calan) o Type II – Dihydropyridines: do not affect conduction through the AV node Nifedipine (Procardia), amlopidine (Norvasc), felodipine (Plendil) Cardiac Glycosides Nitrates • amyl nitrate • isosorbide dinitrate • isosorbide mononitrate • nitrogylcerin
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