作者: Gregory C. Amberg , L. Fernando Santana
DOI: 10.1161/01.RES.0000100068.43006.36
关键词: BK channel 、 Endocrinology 、 Patch clamp 、 Vasoconstriction 、 Vascular smooth muscle 、 Iberiotoxin 、 Genetic model 、 Chemistry 、 Potassium channel 、 Internal medicine 、 Ryanodine receptor
摘要: The molecular mechanisms underlying increased arterial tone during hypertension are unclear. In vascular smooth muscle, localized Ca 2+ release events through ryanodine-sensitive channels located in the sarcoplasmic reticulum (Ca sparks) activate large-conductance, -sensitive K + (BK) channels. sparks and BK provide a negative feedback mechanism that hyperpolarizes muscle thereby opposes vasoconstriction. this study, we examined channel function Wistar-Kyoto (WKY) rats with borderline spontaneously hypertensive (SHR), widely used genetic model of severe hypertension. We found amplitude spontaneous currents WKY SHR cells were smaller than normotensive even though similar magnitude. less sensitive to physiological changes intracellular cells. Our data indicate decreased expression β1 subunit underlies lower sensitivity myocytes. conclude reduced activity by decreasing these . These results support view composition may be fundamental event contributing development dysfunction