José F Bernardo, Clara E Magyar, W Bruce Sneddon, Peter A Friedman
Department of Medicine, Renal Electrolyte Division, W1340 Biomedical Science Tower, Pittsburgh, PA 15261, USA.
Canadian journal of physiology and pharmacology 2009 JulTransgenic mice lacking calcium channel beta3 subunits (CaVbeta3) were used to determine the involvement of a multimeric calcium channel in mediating stimulated renal calcium absorption. We measured the ability of calcium channel beta3 subunit-null (CaVbeta3-/-) and wild-type (CaVbeta3+/+) mice to increase renal calcium absorption in response to the calcium-sparing diuretic chlorothiazide (CTZ). Control rates of fractional sodium excretion were comparable in CaVbeta3-/- and CaVbeta3+/+ mice and CTZ increased sodium excretion similarly in both groups. CTZ enhanced calcium absorption only in wild-type CaVbeta3+/+ mice. This effect was specific for diuretics acting on distal tubules because both CaVbeta3-/- and CaVbeta3+/+ mice responded comparably to furosemide. The absence of beta3 subunits resulted in compensatory increases of TrpV5 calcium channels, the plasma membrane Ca-ATPase, NCX1 Na/Ca exchanger protein, and calbindin-D9k but not calbindin-D28k. We conclude that TrpV5 mediates basal renal calcium absorption and that a multimeric calcium channel that includes CaVbeta3 mediates stimulated calcium transport.
José F Bernardo, Clara E Magyar, W Bruce Sneddon, Peter A Friedman. Impaired renal calcium absorption in mice lacking calcium channel beta 3 subunits. Canadian journal of physiology and pharmacology. 2009 Jul;87(7):522-30
PMID: 19767875
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