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This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/H923    most recent 01126.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Brueggemann, L. I. Articles by Cribbs, L. L. Search for Related Content PubMed PubMed Citation Articles by Brueggemann, L. I. Articles by Cribbs, L. L.

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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