High impact information on Kcnmb1

• Using immunohistochemical techniques, we found that BK-beta1 was strongly expressed in the apical membrane of the murine distal nephron and that 98% of BK-beta1 protein detected by histochemistry colocalized with NCX, a marker of connecting tubules (CNT) [1].
• Potassium chloride- and iberiotoxin-induced depolarization mimicked the effect of BKbeta1-deletion by increasing vascular O2- in an NADPH-dependent fashion [2].
• NADPH oxidase accounts for enhanced superoxide production and impaired endothelium-dependent smooth muscle relaxation in BKbeta1-/- mice [2].
• We propose that the elevated blood pressure in BKbeta1 -/- mice serves to normalize Ca(2+) spark/STOC coupling for regulating myogenic tone [3].
• BK channels are composed of channel-forming BKalpha and auxiliary BKbeta1 subunits, which confer to BK channels an increased sensitivity for changes in membrane potential and Ca(2+) [3].

Biological context of Kcnmb1

• BKbeta1 -/- mice had higher systemic blood pressure than BKbeta1 +/+ mice but responded normally to alpha(1)-adrenergic vasoconstriction and nitric oxide-mediated vasodilation [3].

Anatomical context of Kcnmb1

• Cerebral artery VSMCs from BKbeta1 -/- mice generated Ca(2+) sparks of normal amplitude and frequency, but STOC frequencies were largely reduced at physiological membrane potentials [3].

Associations of Kcnmb1 with chemical compounds

• These data show that the BK-beta1 accessory subunit is present in the CNT segment of the mammalian distal nephron and has a significant role in the kaliuretic response to increased urinary flow induced by volume expansion [1].
• Because the BK-beta1 subunit enhances Ca(2+) sensitivity of BK in a variety of cells, we determined its role in flow-induced K(+) secretion and its localization in the mammalian nephron [1].
• CONCLUSIONS: The deletion of BKbeta1 causes endothelial dysfunction by increasing O2- formation via increasing activity and expression of the vascular NADPH oxidase [2].

References