PHAR 100 Study Guide - Final Guide: Ace Inhibitor, Monoamine Oxidase Inhibitor, Muscarinic Acetylcholine Receptor

• School: Queen's University
• Department: Pharmacology and Toxicology
• Course: PHAR 100
• Professor: Bill Racz

Document Summary

Gtn is converted to nitric oxide an endogenous vasodilator. Binds to guanyly cyclase and triggers a series of events that relaxes vascular smooth muscle. Dilates large veins decreases venous blood returning to the heart = decrease in cardiac output. = decrease in bp and less o2 is needed. Dilates arteries to increase and divert blood flow to areas of deficient o2. Rapid effect that reaches max response in 5 minutes when administered sublingually (also no tolerance develops with this method) Several attacks use isosorbide dinitrate or transdermal gtn. Damage to blood vessels in vital organs such as kidney, heart, and brain. Causing stroke, heart attack, renal failure and vascular disease. Angiotensin converting enzyme inhibitor: captopril inhibit the conversion of angiotensin i to angiotensin ii (potent hypertensive, leading to less angiotensin ii = less constriction of blood vessels and inhibits the mediated aldosterone release. Patients demand antibiotics putting pressure on physicians. Sold inappropriately as otc in foreign countries.