AJP - Renal Physiology, Vol 260, Issue 5 757-F763, Copyright © 1991 by American Physiological Society
Vitamin D3 metabolites increase [Ca2+]i in rabbit renal proximal straight tubule cells
M. Suzuki, S. Kurihara, Y. Kawaguchi and O. Sakai
Second Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.
Vitamin D metabolites exert both acute and chronic influences on proximal
tubule function. To further evaluate vitamin D action on the kidney, we
examined the immediate effects of vitamin D metabolites on cytoplasmic
calcium ion concentration [( Ca2+]i), using fura-2 and patch-clamp method
in cultured proximal straight tubule cells of rabbit kidney.
1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] and 25-hydroxyvitamin D3 [25(OH)D3]
evoked a transient rise in [Ca2+]i, and 24,25-dihydroxyvitamin D3
[24,25(OH)2D3] caused a sustained rise in [Ca2+]i; all effects were dose
dependent. [Ca2+]i transient, evoked by 1,25(OH)2D3 alone, was abolished in
Ca(2+)-free media. Pretreatment of cells in Ca(2+)-free media with caffeine
(4 mM) or ryanodine (1 microM) to deplete Ca2+ store of endoplasmic
reticulum or with TMB-8 (5 mM) to block Ca2+ release from storage blunted
the effect of 25(OH)D3 on [Ca2+]i but not of 24,25(OH)2D3. Data were also
supported by activities of Ca-dependent K channel and show that these three
vitamin D metabolites in pharmacological doses increase [Ca2+]i of proximal
tubule cells from different sources.
