Phelan E L, Simpson F O
Wellcome Medical Research Institute, University of Otago Medical School, Dunedin, New Zealand.
J Hypertens Suppl. 1988 Dec;6(4):S681-3. doi: 10.1097/00004872-198812040-00214.
Verapamil, a calcium-entry blocker, and sodium nitroprusside, a non-specific vasodilator, were infused into the blood-perfused hindlimbs of New Zealand genetically hypertensive rats (NZGH) and spontaneously hypertensive rats (SHR), two genetic models of hypertension, and their normotensive controls, New Zealand normotensive rats and Wistar-Kyoto rats (WKY). Vasodilator responses, measured as the falls in perfusion pressure from the initial values, were similar and increased in NZGH and SHR. The responses were strongly dependent on the initial level of perfusion pressure in each strain of rat. It is concluded that increased vascular resistance, rather than a qualitative difference in vasodilator mechanisms, accounts for the enhanced responses to verapamil and sodium nitroprusside in NZGH and SHR hindlimbs.
维拉帕米（一种钙通道阻滞剂）和硝普钠（一种非特异性血管扩张剂）被注入新西兰遗传性高血压大鼠（NZGH）和自发性高血压大鼠（SHR）这两种高血压遗传模型及其血压正常的对照动物——新西兰血压正常大鼠和Wistar-Kyoto大鼠（WKY）的血液灌注后肢中。以灌注压相对于初始值的下降来衡量的血管扩张反应在NZGH和SHR中相似且增强。这些反应强烈依赖于每种大鼠品系的初始灌注压水平。得出的结论是，血管阻力增加而非血管扩张机制的质的差异导致了NZGH和SHR后肢对维拉帕米和硝普钠的反应增强。
