HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 580/2/523    most recent jphysiol.2006.126128v1 Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Nikitina, E. Articles by Macdonald, R. L. Search for Related Content PubMed PubMed Citation Articles by Nikitina, E. Articles by Macdonald, R. L. Related Collections Cardiovascular

¹ Section of Neurosurgery, Department of Surgery, University of Chicago Medical Center and Pritzker School of Medicine, Chicago, IL, USA
² Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, Ukraine

Electrophysiological and molecular characteristics of voltage-dependent calcium (Ca²⁺) channels were studied using whole-cell patch clamp, polymerase chain reaction and Western blotting in smooth muscle cells freshly isolated from dog basilar artery. Inward currents evoked by depolarizing steps from a holding potential of –50 or –90 mV in 10 mM barium consisted of low- (LVA) and high-voltage activated (HVA) components. LVA current comprised more than half of total current in 24 (12%) of 203 cells and less than 10% of total current in 52 (26%) cells. The remaining cells (127 cells, 62%) had LVA currents between one tenth and one half of total current. LVA current was rapidly inactivating, slowly deactivating, inhibited by high doses of nimodipine and mibefradil (> 0.3 µM), not affected by -agatoxin GVIA (100 nM), -conotoxin IVA (1 µM) or SNX-482 (200 nM) and probably carried by T-type Ca²⁺ channels based on the presence of messenger ribonucleic acid (mRNA) and protein for Ca_v3.1 and Ca_{v3.3 1} subunits of these channels. LVA currents exhibited window current with a maximum of 13% of the LVA current at –37.4 mV. HVA current was slowly inactivating and rapidly deactivating. It was inhibited by nimodipine (IC₅₀ = 0.018 µM), mibefradil (IC₅₀ = 0.39 µM) and -conotoxin IV (1 µM). Smooth muscle cells also contained mRNA and protein for L- (Ca_v1.2 and Ca_v1.3), N- (Ca_v2.2) and T-type (Ca_v3.1 and Ca_v3.3) ₁ Ca²⁺ channel subunits. Confocal microscopy showed Ca_v1.2 and Ca_v1.3 (L-type), Ca_v2.2 (N-type) and Ca_v3.1 and Ca_v3.3 (T-type) protein in smooth muscle cells. Relaxation of intact arteries under isometric tension in vitro to nimodipine (1 µM) and mibefradil (1 µM) but not to -agatoxin GVIA (100 nM), -conotoxin IVA (1 µM) or SNX-482 (1 µM) confirmed the functional significance of L- and T-type voltage-dependent Ca²⁺ channel subtypes but not N-type. These results show that dog basilar artery smooth muscle cells express functional voltage-dependent Ca²⁺ channels of multiple types.

(Received 5 December 2006; accepted after revision 19 December 2006; first published online 21 December 2006)
Corresponding author R. L. Macdonald: Division of Neurosurgery, St Michael's Hospital University of Toronto, 30 Bond Street, Toronto, ON, Canada, MSB 1W8.   Email: Macdonaldlo{at}smh.toronto.on.ca

This article has been cited by other articles:

				M. F. Navedo, G. C. Amberg, R. E. Westenbroek, M. J. Sinnegger-Brauns, W. A. Catterall, J. Striessnig, and L. F. Santana Cav1.3 channels produce persistent calcium sparklets, but Cav1.2 channels are responsible for sparklets in mouse arterial smooth muscle Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1359 - H1370. [Abstract] [Full Text] [PDF]