Cilnidipine: Preclinical Profile and Clinical Evaluation
Cilnidipine: Preclinical Profile and Clinical Evaluation
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西尼地平：临床前概况和临床评价
DOI：
10.1111/j.1527-3466.1999.tb00024.x
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
R. Yoshimoto
中科院分区：
文献类型：
--
作者：
H. Uneyama;H. Uchida;T. Konda;R. Yoshimoto
通道和神经细胞在N型钙通道水平。西尼地平的L型钙通道阻滞剂主要作用于血管平滑肌，从而引起外周阻力血管和冠状动脉的扩张。N型钙通道的阻断主要影响交感神经元的外周神经末梢，从而通过降低血浆儿茶酚胺水平来扩张血管。与健康志愿者相比，西尼地平对高血压患者的降压作用更大。虽然在传统的L类选择性DHP的研究中注意到心率的增加，但西尼地平对心率的改变可以忽略不计，即使在快速降压的患者中也是如此。因此，低血压引起的压力感受性交感神经刺激可能被这种对N型钙离子的抑制作用减弱。
channels and neuronal cells at the level of N-type Ca 2+ channels. The L-type Ca 2+ channel blockade by cilnidipine affects predominantly vascular smooth muscle, thereby producing vasodilation of peripheral resistance vessels and coronary arteries. The blockade of N-type Ca channels affects predominantly peripheral nerve endings of sympathetic neurons, thereby dilating blood vessels by lowering plasma catecholamine levels. Cilnidipine produced greater reductions in blood pressure in patients with hypertension than in healthy volunteers. Although increases in heart rate were noted in studies with conventional L-type selective DHPs, the changes in heart rate with cilnidipine were negligible, even in patients with rapid blood pressure reduction. Thus, it appears that the hypotension-induced baroreflex sympathetic stimulation is attenuated by this inhibitory action on N-type Ca 2+