Triggle C R, Tabrizchi R
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Calgary, Alberta, Canada.
Chin Med J (Engl). 1993 Apr;106(4):250-7.
In a comparison of the spontaneously hypertensive rat (SHR) with Wistar-Kyoto (WKY) and Sprague Dawley (SD) rats, it was shown that pertussis toxin (PTX) lowers the blood pressure of the SH but not WKY or SD rats. Sympathetic nerve stimulation (SNS), via the pithing rod, the nitric oxide NO)-synthase inhibitor NW-Nitro-L-arginine methyl ester L-NAME) and the pressor response to infusion of AVP were also observed. The results indicate that a G-protein(s) population and/or function may be altered in the vascular smooth muscle of SH rats. This dysfunction may contribute to the heightened pressor responsiveness of the SHR vasculature to SNS and arginine vasopressin (AVP) and the increased sensitivity to the hypotensive effects of nifedipine. NO-synthase activity also appears to be increased in the SHR, suggesting that this increase should reflect a compensatory change due to the elevation of BP in SHR.
在将自发性高血压大鼠(SHR)与Wistar-Kyoto(WKY)大鼠和Sprague Dawley(SD)大鼠进行比较时发现,百日咳毒素(PTX)可降低SHR的血压,但对WKY大鼠或SD大鼠无效。还观察了通过脊髓穿刺棒进行的交感神经刺激(SNS)、一氧化氮(NO)合酶抑制剂Nω-硝基-L-精氨酸甲酯(L-NAME)以及对输注血管加压素(AVP)的升压反应。结果表明,SHR大鼠血管平滑肌中的一种或多种G蛋白的数量和/或功能可能发生了改变。这种功能障碍可能导致SHR血管系统对SNS和精氨酸血管加压素(AVP)的升压反应增强,以及对硝苯地平降压作用的敏感性增加。SHR中的NO合酶活性似乎也有所增加,这表明这种增加应反映了由于SHR血压升高而产生的代偿性变化。