Masuyama Y, Fukuda K
Department of Medicine, Wakayama Medical College, Japan.
Clin Exp Hypertens A. 1989;11 Suppl 1:31-42. doi: 10.3109/10641968909045410.
Cardiac, aortic and renal alpha- and beta-adrenoceptors were examined in three types of experimental hypertension in rats. In spontaneously hypertensive rats (SHR), cardiac alpha 1-adrenoceptor concentration was increased and cardiac and aortic beta-adrenoceptor concentrations were decreased compared with Wistar-Kyoto rats (WKY). A similar decrease in cardiac beta-adrenoceptor concentration was also shown in two-kidney, one clip (2K, 1C) and deoxycorticosterone acetate(DOCA)-salt hypertensive rats. Renal alpha 1- and alpha 2-adrenoceptor concentrations were increased in SHR, but not in 2K, 1C and DOCA-salt hypertension. In contrast, renal beta-adrenoceptor concentration was increased in 2K, 1C and DOCA-salt hypertension, but unchanged in SHR. The observed increase in cardiac alpha 1- and renal alpha 2-adrenoceptor concentrations may partly contribute to the elevation of blood pressure in SHR.
在三种实验性高血压大鼠模型中,对心脏、主动脉和肾脏的α-及β-肾上腺素能受体进行了检测。与Wistar-Kyoto大鼠(WKY)相比,自发性高血压大鼠(SHR)的心脏α1-肾上腺素能受体浓度升高,而心脏和主动脉β-肾上腺素能受体浓度降低。在二肾一夹(2K,1C)和醋酸脱氧皮质酮(DOCA)-盐性高血压大鼠中,心脏β-肾上腺素能受体浓度也出现类似降低。SHR的肾脏α1-和α2-肾上腺素能受体浓度升高,但在2K,1C和DOCA-盐性高血压模型中未升高。相反,2K,1C和DOCA-盐性高血压模型的肾脏β-肾上腺素能受体浓度升高,而SHR中则无变化。观察到的心脏α1-和肾脏α2-肾上腺素能受体浓度升高可能部分导致了SHR血压升高。