Kusayama T, Yamazaki J, Nagao T
Department of Toxicology and Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Eur J Pharmacol. 1996 Oct 3;312(3):301-7. doi: 10.1016/0014-2999(96)00487-6.
To investigate the flow-dependent contribution of basally released nitric oxide (NO) to vascular perfusion pressure, we compared the effects of a NO synthesis inhibitor on the pressure changes in some models of rate mesenteric vascular beds. Spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats (13-14-weeks-old) were used. The perfusion pressure at each flow rate was slightly higher in the SHR bed than in the WKY bed when no contractile compounds were applied. NG-Monomethyl-L-arginine (L-NMMA) significantly increased the pressure in WKY at flow rates more than 5 ml/min (8.9 mm Hg at 7 ml/min). L-NMMA increased the pressure in SHR at flow rates of 2-7 ml/min (40.2 mm Hg at 7 ml/min). L-NMMA markedly increased the pressure at each flow rate in both beds which methoxamine (30 microM) had constricted. The effects of L-NMMA were concentration-dependent, and were blocked by L-arginine. Therefore, basal NO release appears to contribute to the vasolidating tone although flow dependence of the effect is different in the absence or presence of an exogeneous tone in both hypertensive and normotensive rats.
为了研究基础释放的一氧化氮（NO）对血管灌注压的流量依赖性贡献，我们比较了NO合成抑制剂对一些大鼠肠系膜血管床模型中压力变化的影响。使用自发性高血压（SHR）和血压正常的Wistar Kyoto（WKY）大鼠（13 - 14周龄）。当未应用收缩性化合物时，SHR血管床在每个流速下的灌注压均略高于WKY血管床。NG-单甲基-L-精氨酸（L-NMMA）在流速超过5 ml/min时显著增加WKY的压力（7 ml/min时为8.9 mmHg）。L-NMMA在2 - 7 ml/min的流速下增加SHR的压力（7 ml/min时为40.2 mmHg）。L-NMMA显著增加了甲氧明（30 microM）收缩的两个血管床在每个流速下的压力。L-NMMA的作用呈浓度依赖性，并被L-精氨酸阻断。因此，基础NO释放似乎有助于血管舒张张力，尽管在高血压和血压正常的大鼠中，在无或有外源性张力的情况下，该作用的流量依赖性有所不同。
