Dong Y J, Wadsworth R M
J Cardiovasc Pharmacol. 1986 Nov-Dec;8(6):1176-84. doi: 10.1097/00005344-198611000-00013.
A comparison was made of contractile responses of aortic rings isolated from rabbits with perinephritis hypertension and sham-operated rabbits. Contraction was elicited by potassium, noradrenaline or 11,9-epoxymethano PGH2 (a thromboxane A2 mimetic). Except for the maximum response to noradrenaline, there were no significant differences in the responses to KCl or 11,9-epoxymethano PGH2 between normotensive and hypertensive rabbit aorta preparations. Hypertensive rabbit aorta preparations were more susceptible to the calcium channel inhibitors nifedipine and nisoldipine, but less sensitive to a calcium channel facilitator Bay K 8644 than were normotensive preparations. These results suggest that calcium regulatory mechanisms undergo changes during the development of hypertension. We have also found that nifedipine and nisoldipine show high inhibitory potency in the calcium channel inhibitor-sensitive contractile component during alpha-adrenoceptor activation and appear to be weak competitive antagonists at thromboxane A2 receptor sites.
对从患有肾周炎高血压的兔子和假手术兔子分离出的主动脉环的收缩反应进行了比较。通过钾、去甲肾上腺素或11,9-环氧甲撑PGH2（一种血栓素A2模拟物）引发收缩。除了对去甲肾上腺素的最大反应外，正常血压和高血压兔子主动脉制剂对氯化钾或11,9-环氧甲撑PGH2的反应没有显著差异。高血压兔子主动脉制剂比正常血压制剂对钙通道抑制剂硝苯地平和尼索地平更敏感，但对钙通道促进剂Bay K 8644的敏感性较低。这些结果表明，在高血压发展过程中钙调节机制会发生变化。我们还发现，硝苯地平和尼索地平在α-肾上腺素能受体激活期间对钙通道抑制剂敏感的收缩成分显示出高抑制效力，并且在血栓素A2受体部位似乎是弱竞争性拮抗剂。
