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Functional role of voltage‐gated Na+ channels in rat mesenteric arteries
Author(s) -
Ho Vanessa,
Davis Alison,
Greenwood Iain
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1026.7
Subject(s) - myograph , veratridine , contractility , tetrodotoxin , mesenteric arteries , electrical impedance myography , vascular smooth muscle , activator (genetics) , chemistry , medicine , endocrinology , anatomy , sodium channel , artery , vasodilation , smooth muscle , receptor , sodium , organic chemistry
We have previously reported that voltage‐gated Na + channels (Na V ) are expressed in freshly dissociated smooth muscle cells from the mouse portal vein, which displays spontaneous, rhythmic contractions. However, the physiological function of Na V in smooth muscle is controversial. Here, we explored the role of Na V in arterial vascular contractility. Isolated mesenteric arteries from male Wistar rats (200–300g) were mounted in a wire‐myograph for tension recording. The Na V activator veratridine elicited concentration‐dependent (1–30μM), but endothelium‐independent, contractions. These contractions (at 10μM, 8.8±0.7mN; n=8) were greatly inhibited by 1μM tetrodotoxin (TTX), a Na V blocker (1.3±0.9mN, n=4) and abolished in Na + ‐free physiological salt solution (−0.2±0.1mN, n=4). To probe the expression of Na V isoforms (Na V 1.1–1.9), we used conventional reverse transcriptase polymerase chain reaction (RT‐PCR) with mRNA extracted from the isolated vessels. The presence of TTX‐sensitive Na V isoforms (1.2, 1.3, 1.6 and 1.7) was evident. Based on these data, we propose that functional Na V are expressed in arteries without spontaneous rhythmic contractions and may play a role in the regulation of vascular tone. We acknowledge the financial support from St George's University of London and British Heart Foundation