Sakai K, Akima M, Saito K
Central Research Laboratories, Chugai Pharmaceutical Co. Ltd, Tokyo, Japan.
J Pharm Pharmacol. 1998 Feb;50(2):211-4. doi: 10.1111/j.2042-7158.1998.tb06178.x.
The effects of nicorandil on vasodepressor responses to vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) and substance P have been examined in anaesthetized rats. Intravenous bolus injections of VIP (0.3 microg kg(-1)), CGRP (0.1 microg kg(-1)) and substance P (0.1 microg kg(-1)) induced reductions of blood pressure accompanied by slight increases (less than 5%) in heart rate. Nicorandil infused intravenously at 10 or 30 microg kg(-1) min(-1) significantly augmented the vasodepressor responses to VIP and CGRP but did not modify the responses to substance P and acetylcholine (0.1 microg kg(-1)). Intravenous treatment with glibenclamide (20 mg kg(-1)) [corrected] significantly attenuated not only the vasodepression caused by VIP and CGRP, but also the enhancement of the effects of the agents by nicorandil. These results indicate that nicorandil can enhance the action of VIP and CGRP, in rats, at least partly through ATP-sensitive K+-channel activation.
在麻醉大鼠中研究了尼可地尔对血管活性肠肽（VIP）、降钙素基因相关肽（CGRP）和P物质引起的血管减压反应的影响。静脉推注VIP（0.3μg kg⁻¹）、CGRP（0.1μg kg⁻¹）和P物质（0.1μg kg⁻¹）可导致血压降低，同时心率略有增加（小于5%）。以10或30μg kg⁻¹ min⁻¹的速度静脉输注尼可地尔可显著增强对VIP和CGRP的血管减压反应，但不改变对P物质和乙酰胆碱（0.1μg kg⁻¹）的反应。静脉注射格列本脲（20mg kg⁻¹）不仅显著减弱了由VIP和CGRP引起的血管减压作用，而且减弱了尼可地尔对这些药物作用的增强作用。这些结果表明，在大鼠中，尼可地尔至少部分通过激活ATP敏感性钾通道来增强VIP和CGRP的作用。
