Wistar-Kyoto大鼠和自发性高血压大鼠中的血管蛋白激酶C
Vascular protein kinase C in Wistar-Kyoto and spontaneously hypertensive rats.
作者信息
Silver P J, Cumiskey W R, Harris A L
机构信息
Department of Cardiovascular Pharmacology, Sterling Winthrop Pharmaceuticals Research Division, Rensselaer, NY 12144.
出版信息
Eur J Pharmacol. 1992 Mar 3;212(2-3):143-9. doi: 10.1016/0014-2999(92)90322-u.
Phorbol esters which activate protein kinase C (PKC) produced concentration-related force development in aorta from spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY); all were 2-7 x more potent in SHR. However, total PKC activity in aortas, as well as carotid, caudal and renal arteries, was not different, when SHR was compared with WKY. Binding of phorbol dibutyrate to particulate aortic PKC was similar in SHR and WKY (same apparent Kd and Bmax values), as was potency for displacement of phorbol dibutyrate by phorbol myristate acetate. Furthermore, there was no difference in potency with staurosporine, H-7, and calmidazolium in inhibiting SHR and WKY aortic PKC. These data demonstrate enhanced contractile sensitivity to PKC-activating phorbol esters in SHR aortic smooth muscle that is not related to activity, phorbol ester binding, or sensitivity to inhibitors when SHR PKC is compared with WKY PKC. Thus, signal transduction events distal to PKC activation may be responsible for enhanced vascular contractile sensitivity to phorbol esters in SHR.
激活蛋白激酶C（PKC）的佛波酯在自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）的主动脉中产生了浓度相关的力量发展；在SHR中，所有佛波酯的效力都高2至7倍。然而，将SHR与WKY相比时，主动脉以及颈动脉、尾动脉和肾动脉中的总PKC活性并无差异。在SHR和WKY中，佛波二丁酸酯与主动脉微粒体PKC的结合相似（表观Kd和Bmax值相同），佛波肉豆蔻酸酯乙酸盐置换佛波二丁酸酯的效力也是如此。此外，在抑制SHR和WKY主动脉PKC方面，星形孢菌素、H-7和氯咪达唑的效力没有差异。这些数据表明，与WKY PKC相比，SHR主动脉平滑肌对PKC激活佛波酯的收缩敏感性增强，这与活性、佛波酯结合或对抑制剂的敏感性无关。因此，PKC激活远端的信号转导事件可能是SHR中血管对佛波酯收缩敏感性增强的原因。
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