AJP - Renal Physiology, Vol 267, Issue 1 183-F189, Copyright © 1994 by American Physiological Society

ARTICLES

Ca(2+)-dependent activation of T-type Ca2+ channels by calmodulin-dependent protein kinase II

H. K. Lu, R. J. Fern, J. J. Nee and P. Q. Barrett
Department of Pharmacology, University of Virginia, Charlottesville 22908.

The T-type Ca2+ channel is unique among voltage-dependent Ca2+ channels in its low threshold for opening and its slow kinetics of deactivation. Here, we evaluate the importance of intracellular Ca2+ (Cai2+) in promoting low-threshold gating of T-type channels in adrenal glomerulosa cells. We observe that 390 nM to 1.27 microM Cai2+ enhances T-type current by shifting the voltage dependence of channel activation to more negative potentials. This Ca(2+)-induced shift is mediated by calmodulin-dependent protein kinase II (CaMKII), because it is abolished by inhibitors of CaMKII but not of protein kinase C and is subsequently restored by exogenous calmodulin. This Ca(2+)-induced reduction in gating threshold would render T-type Ca2+ channels uniquely suited to transduce depolarizing stimuli of low amplitude into a Ca2+ signal sufficient to support a physiological response.

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