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Am J Physiol Heart Circ Physiol (October 21, 2004). doi:10.1152/ajpheart.01126.2003
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Submitted on November 26, 2003
Accepted on October 14, 2004

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

Lioubov I. Brueggemann1, Beverly L. Martin1, John Barakat1, Kenneth L. Byron1, and Leanne L. Cribbs1*

1 Medicine, Cardiovascular Institute, Loyola University Medical Center, Maywood, IL, USA

* To whom correspondence should be addressed. E-mail: lcribbs{at}lumc.edu.

An important path of extracellular calcium influx in vascular smooth muscle (VSM) cells is through voltage activated calcium channels of the plasma membrane. Both high (HVA) and low voltage-activated (LVA) 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. Arginine vasopressin (AVP) is a vasoconstrictor hormone that, at physiological concentrations, stimulates Ca2+ oscillations (spiking) in monolayer cultures of A7r5 cells. The present study investigates the role of T-type Ca2+ channels in this response using 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 Cav3.2 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.




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