tailieunhanh - Color Atlas of Pharmacology (Part 11): Vasodilators

Vasodilators alogues such as iloprost, or prostaglandin E1 analogues such as alprostanil, mimic the actions of relaxant mediators. Ca2+ antagonists reduce depolarizing inward Ca2+ currents, while K+-channel activators promote outward (hyperpolarizing) K+ currents. Organic nitrovasodilators give rise to NO, an endogenous activator of guanylate cyclase. Individual vasodilators. Nitrates (p. 120) Ca2+-antagonists (p. 122). "1antagonists (p. 90), ACE-inhibitors, AT1antagonists (p. 124); and sodium nitroprusside (p. 120) are discussed elsewhere. Dihydralazine and minoxidil (via its sulfate-conjugated metabolite) dilate arterioles and are used in antihypertensive therapy. They are, however, unsuitable for monotherapy because of compensatory circulatory reflexes. . | 118 Vasodilators Vasodilators-Overview The distribution of blood within the circulation is a function of vascular caliber. Venous tone regulates the volume of blood returned to the heart hence stroke volume and cardiac output. The luminal diameter of the arterial vasculature determines peripheral resistance. Cardiac output and peripheral resistance are prime determinants of arterial blood pressure p. 314 . In A the clinically most important vasodilators are presented in the order of approximate frequency of therapeutic use. Some of these agents possess different efficacy in affecting the venous and arterial limbs of the circulation width of beam . Possible uses. Arteriolar vasodilators are given to lower blood pressure in hypertension p. 312 to reduce cardiac work in angina pectoris p. 308 and to reduce ventricular afterload pressure load in cardiac failure p. 132 . Venous vasodilators are used to reduce venous filling pressure preload in angina pectoris p. 308 or cardiac failure p. 132 . Practical uses are indicated for each drug group. Counter-regulation in acute hypotension due to vasodilators B . Increased sympathetic drive raises heart rate reflex tachycardia and cardiac output and thus helps to elevate blood pressure. Patients experience palpitations. Activation of the renin-angioten-sin-aldosterone RAA system serves to increase blood volume hence cardiac output. Fluid retention leads to an increase in body weight and possibly edemas. These counter-regulatory processes are susceptible to pharmacological inhibition p-blockers ACE inhibitors AT1-antagonists diuretics . Mechanisms of action. The tonus of vascular smooth muscle can be decreased by various means. ACE inhibitors antagonists at AT1-receptors and antagonists at -adrenoceptors protect against the effects of excitatory mediators such as angiotensin II and norepinephrine respectively. Prostacyclin an alogues such as iloprost or prostaglandin E1 analogues such as alprostanil mimic the actions of relaxant