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

Open Access
Publisher Website
Google Scholar
Abstract
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 (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.