抗心绞痛药V.ppt

其他抗心绞痛药物 卡维地洛：去甲肾上腺素能神经受体阻断药，又具有抗氧化作用。用于心绞痛、心功能不全和高血压治疗。 雷诺嗪 * Mechanism of action of nitrates, nitrites, and other substances that increase the concentration of nitric oxide (NO) in vascular smooth muscle cells. Steps leading to relaxation are shown with blue arrows. MLCK*, activated myosin light-chain kinase. Nitrosothiols (SNOs) appear to have non-cGMP-dependent effects on potassium channels and Ca2+-ATPase. GC*, activated guanylyl cyclase; PDE,phosphodiesterase; eNOS, endothelial nitric oxide synthase; mtALDH2, mitochondrial aldehyde dehydrogenase-2; ROCK, Rho kinase. * * A simplified diagram of smooth muscle contraction and the site of action of calcium channel-blocking drugs. Contraction is triggered (red arrows) by influx of calcium (which can be blocked by calcium channel blockers) through transmembrane calcium channels. The calcium combines with calmodulin to form a complex that converts the enzyme myosin light-chain kinase to its active form (MLCK*). The latter phosphorylates the myosin light chains, thereby initiating the interaction of myosin with actin. Other proteins, including calponin and caldesmon (not shown), inhibit the ATPase activity of myosin during the relaxation of smooth muscle. Interaction with the Ca2+-calmodulin complex reduces their interaction with myosin during the contraction cycle. Beta2 agonists (and other substances that increase cAMP) may cause relaxation in smooth muscle (blue arrows) by accelerating the inactivation of MLCK and by facilitating the expulsion of calcium from the cell (notshown). cGMP facilitates relaxation by the mechanism shown in Figure 12–2. ROCK, Rho kinase. * Vasodilators theTreatment ofAngina Pectoris Introduction The name angina pectoris denotes chest paincaused by accumulation of metabolites resulting from myocardial ischemia. 临床表现：阵发性的胸骨后压榨性疼痛并向左上肢放射。 2. classfication 劳累性心绞痛：心肌耗氧量增加时诱发。休息或硝酸甘油可以缓解。 自发性心绞痛：与心肌耗氧量无明显关系。安静时也可以发生。硝酸甘油不能缓解。 混合性心绞痛 PATHOPHYSIOLOGY OF ANGINA Determinants of Myocardial