【文章內(nèi)容簡介】 e young （年輕人和白人） ? Mechanisms of action include: – 1) decrease myocardial contractility and CO。 – 2) decrease renin secretion and hence decrease levels of angiotensin II – 3)block presynaptic receptors and inhibit the release of NE from the terminal of nerves propranolol, metoprolol, atenolol 脂溶性強藥物效果比水溶性強藥物好（ metoprolol, atenolol） ? Side Effects of Most BetaBlockers: mild chronic fatigue, low exercise tolerance, sedation, nightmares, increased airway resistance, bradycardia ? Therapeutic Notes: – betablockers must be withdrawn gradually to avoid withdrawal – betablockers are roughly equivalent in efficacy as antihypertensive agents – betablockers may mask insulininduced hypoglycemia LType Calcium Channel Blockers ? More effect for the black and the older （老年人和黑人） ? Primary Mechanisms of Action: inhibit Ca++ influx into vascular smooth muscle。 relax peripheral arteriole smooth muscle and thereby decrease total peripheral resistance。 interfere with both angiotensin II and alpha2mediated vasocontriction, and perhaps alpha1mediated vasoconstriction. ? Nifedipine, nitridipine, amlodipine, felodipine etc dihydropyridines。 relatively selective vasodilator and less cardiac depression than verapamil or diltiazem – Side Effects: tachycardia, headache, peripheral edema, flushing ? Diltiazem (Cardizem) intermediate action on heart and blood vessels – Side Effects: dizziness, headache, edema, bradycardia ? Verapamil (Calan) greatest effect on heart – Side Effects: dizziness, headache, edema, constipation, bradycardia ? Therapeutic Notes: ? Ca++ channel blockers are only rarely associated with abnormalities in electrolyte, carbohydrate, or lipid metabolism. The drugs do not alter plasma concentrations of uric acid. ? Ca++ channel blockers are useful in hypertensive patients with a wide variety of conitant illnesses including ischemic heart disease, chronic pulmonary disease, diabetes mellitus and variant angina. 不適用于心衰病人。 Angiotensin Converting Enzyme (ACE) Inhibitors ? Primary Mechanisms of Action: inhibit production of angiotensin II (vasoconstriction and sodiumretaining activity)。 decrease total peripheral resistance 血管緊張素原 AngiotensinⅠ 收縮血管 腎素 激肽原 緩激肽 ↑ 降解失活 AngⅢ ACE 糜酶 ACEIs AngⅡ ↓ 分泌醛固酮 NO PGI ( ) ACE和 ACEIs作用示意圖 舒張血管 ? Side Effects of ACE Inhibitors: hyperkalemia, rash, dry cough, angioneurotic edema (% cases) ? Therapeutic Note: contraindicated in second and third trimesters of pregnancy 損傷胚胎 Angiotensin II antagonists (ARBs) ? Angiotensin II receptor antagonists are effective in lowering the blood pressure of hypertensives and are useful in bination with diuretics. The drugs may be useful in those patients who have unacceptable ACE inhibitorinduced cough. However, to what extent they may share the benefits of ACE inhibitors in hypertensive patients with congestive heart failure or type I diabetes is not yet known. 藥物治療原則 ? 從小劑量開始，逐漸加量至合適劑量?？蓽p少不良反應(yīng)。 ? 長效制劑，給藥一天一次，早上服用。增加病人用藥依從性。 ? 聯(lián)合用藥（合并用藥）。 聯(lián)合用藥 ? 高血壓病發(fā)病因素復(fù)雜，單種藥物治療常常不能很好控制血壓，因而常合并使用 2至 3種藥物用于抗高血壓。不同作用機制的藥物合用后產(chǎn)生協(xié)同或相加的抗高血壓作用。減少單藥用量，降低不良反應(yīng)的發(fā)生。 ? D+B， D+ACEI， D+ARB ? B+C ? ACEI+ARB 治療冠心病藥物 Agents to treat CHD coronary heart disease ? Background: IHD is the leading single cause of death in the US and is responsible for 1 of every deaths. About half of the patients with IHD initially present with chronic stable angina. IHD manifests as an imbalance in myocardial oxygen supply and demand that results in myocardial hypoxemia. IHD is usually due to atherosclerotic disease of the coronary arteries (coronary heart disease [CHD] and coronary artery disease [CAD])。 病因?qū)W Etiology ? The exact pathogenesis of CAD is not clear, and no single theory adequately explains the atheroscler