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Low voltage-activated calcium channels in vascular smooth muscle: T-type channels and AVP-stimulated calcium spiking

Department of Medicine, Cardiovascular Institute, Loyola University Medical Center, Maywood, Illinois

Submitted 26 November 2003 ; accepted in final form 14 October 2004

An important path of extracellular calcium influx in vascular smooth muscle (VSM) cells is through voltage-activated Ca²⁺ channels of the plasma membrane. Both high (HVA)- and low (LVA)-voltage-activated Ca²⁺ currents are present in VSM cells, yet little is known about the relevance of the LVA T-type channels. In this report, we provide molecular evidence for T-type Ca²⁺ channels in rat arterial VSM and characterize endogenous LVA Ca²⁺ currents in the aortic smooth muscle-derived cell line A7r5. AVP is a vasoconstrictor hormone that, at physiological concentrations, stimulates Ca²⁺ oscillations (spiking) in monolayer cultures of A7r5 cells. The present study investigated the role of T-type Ca²⁺ channels in this response with a combination of pharmacological and molecular approaches. We demonstrate that AVP-stimulated Ca²⁺ spiking can be abolished by mibefradil at low concentrations (<1 µM) that should not inhibit L-type currents. Infection of A7r5 cells with an adenovirus containing the Ca_v3.2 T-type channel resulted in robust LVA Ca²⁺ currents but did not alter the AVP-stimulated Ca²⁺ spiking response. Together these data suggest that T-type Ca²⁺ channels are necessary for the onset of AVP-stimulated calcium oscillations; however, LVA Ca²⁺ entry through these channels is not limiting for repetitive Ca²⁺ spiking observed in A7r5 cells.

calcium; Ca_v3.1; Ca_v3.2; arterial myocytes

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