Saito K, Sakai K
Central Research Laboratories, Chugai Pharmaceutical Co., Ltd., Tokyo, Japan.
Jpn J Pharmacol. 1998 Feb;76(2):227-31. doi: 10.1254/jjp.76.227.
I.v. bolus injections of vasoactive intestinal polypeptide (VIP) (0.3 or 1 microg/kg), calcitonin gene-related peptide (CGRP) (0.3 microg/kg) or substance P (0.1 microg/kg) to anesthetized rats reduced blood pressure, accompanied by slight increases in heart rate. Cromakalim (0.3 microg/kg/min) infused i.v. significantly potentiated the depressor responses to VIP and CGRP, but not those to substance P and acetylcholine (ACh) (0.1 microg/kg). Glibenclamide (20 mg/kg, i.v.) significantly inhibited not only the depressor responses to VIP and CGRP, but also the augmentation of the effects of the two agents by cromakalim. These results suggest that the depressor responses to VIP and CGRP are mediated in part through K(ATP) channel activation.
对麻醉大鼠静脉推注血管活性肠肽（VIP）（0.3或1微克/千克）、降钙素基因相关肽（CGRP）（0.3微克/千克）或P物质（0.1微克/千克）可降低血压，同时心率略有增加。静脉输注克罗卡林（0.3微克/千克/分钟）可显著增强对VIP和CGRP的降压反应，但对P物质和乙酰胆碱（ACh）（0.1微克/千克）的降压反应无增强作用。格列本脲（20毫克/千克，静脉注射）不仅显著抑制对VIP和CGRP的降压反应，还抑制克罗卡林对这两种药物作用的增强。这些结果表明，对VIP和CGRP的降压反应部分是通过ATP敏感性钾通道激活介导的。
