Modulation of the molecular composition of large conductance, Ca 2+ activated K+ channels in vascular smooth muscle during hypertension

摘要: Hypertension is a clinical syndrome characterized by increased vascular tone. However, the molecular mechanisms underlying dysfunction during acquired hypertension remain unresolved. Localized intracellular Ca2+ release events through ryanodine receptors (Ca2+ sparks) in sarcoplasmic reticulum are tightly coupled to activation of large-conductance, Ca2+-activated K+ (BK) channels provide hyperpolarizing influence that opposes vasoconstriction. In this study we tested hypothesis reduction spark–BK channel coupling underlies smooth muscle hypertension. We found hypertension, expression β1 subunit was decreased relative pore-forming α BK channel. Consequently, were functionally uncoupled from sparks. Consistent with this, contribution tone reduced conclude downregulation contributes These results support novel concept changes composition regulate arterial function.