Downregulation of the BK Channel β1 Subunit in Genetic Hypertension

作者: Gregory C. Amberg , L. Fernando Santana

DOI: 10.1161/01.RES.0000100068.43006.36

关键词: BK channelEndocrinologyPatch clampVasoconstrictionVascular smooth muscleIberiotoxinGenetic modelChemistryPotassium channelInternal medicineRyanodine 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

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