Kwan C Y, Grover A K, Sakai Y
Blood Vessels. 1982;19(6):273-83. doi: 10.1159/000158394.
Microsomal fractions enriched in plasma membranes and endoplasmic reticulum were isolated from stomach fundus and vas deferens from age-matched Okamoto spontaneously hypertensive (SHR) rats and corresponding Kyoto-Wistar normotensive rats (KWR). Alterations of several enzyme activities and Ca2+ accumulation of the isolated microsomal fraction from these nonvascular smooth muscles provide direct evidence of abnormal smooth muscle membrane biochemistry in SHR. Decreased Ca2+ accumulation in the presence of but not in the absence of adenosine triphosphate by the microsomal fractions of both fundus and vas deferens from SHR is consistent with previous findings using plasma membranes from vascular smooth muscles from SHR and cannot be explained in terms of adaptation induced by elevation of blood pressure in SHR. Defective Ca2+ handling now observed in both vascular and nonvascular smooth muscles from hypertensive animals not only provides a cellular basis for the altered reactivity and contractility of smooth muscles observed in SHR, but also supports the hypothesis that spontaneous hypertension is associated with a generalized widespread alteration in smooth muscle membrane fraction.
从年龄匹配的冈本自发性高血压（SHR）大鼠以及相应的京都-威斯塔正常血压大鼠（KWR）的胃底和输精管中分离出富含质膜和内质网的微粒体部分。这些非血管平滑肌分离出的微粒体部分中几种酶活性和Ca2+积累的改变，为SHR中异常的平滑肌膜生物化学提供了直接证据。SHR胃底和输精管的微粒体部分在有三磷酸腺苷存在时Ca2+积累减少，而在无三磷酸腺苷时则不然，这与之前使用SHR血管平滑肌质膜的研究结果一致，且无法用SHR血压升高引起的适应性来解释。现在在高血压动物的血管和非血管平滑肌中均观察到的Ca2+处理缺陷，不仅为SHR中观察到的平滑肌反应性和收缩性改变提供了细胞基础，也支持了自发性高血压与平滑肌膜部分广泛普遍改变相关的假说。
