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Genetic hypertension is associated with an elevation in functional coupling between type 1 IP 3 receptors and TRPC3 channels in arterial smooth muscle cells
Author(s) -
Adebiyi Adebowale,
Leo Marie Dennnis,
Neeb Zachary P,
ThomasGatewood Candice M,
Jaggar Jonathan H
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.819.7
In arterial myocytes, an inositol 1,4,5‐trisphosphate (IP 3 ) elevation stimulates physical coupling between type 1 IP 3 receptors (IP 3 R1) and TRPC3 channels, leading to the activation of a cation current (I Cat ) that induces vasoconstriction. Here, we tested the hypothesis that functional coupling between IP 3 Rs and TRPC channels is modified in mesenteric artery myocytes of genetically hypertensive (SHR) rats. TRPC3 channel expression was similar in mesenteric arteries of pre‐hypertensive (6 wk) SHR and WKY rats. In contrast, TRPC3 channel expression was ~68% higher in hypertensive (13 wk) SHR rat arteries than in age‐matched normotensive Wistar Kyoto (WKY) controls. TRPC1, TRPC6, and IP 3 R1 expression were similar in hypertensive SHR and WKY mesenteric arteries. Surface biotinylation indicated that plasma membrane TRPC3 channel protein was ~44% higher in SHR mesenteric arteries. IP 3 ‐induced I Cat was ~59% larger in SHR than WKY myocytes. ImmunoFRET between IP 3 R1 and TRPC3 channels was ~19% higher in arterial myocytes in SHR than WKY myocytes. These data indicate that hypertension is associated with an increase in mesenteric artery myocyte TRPC3 protein, TRPC3 channel surface expression, and enhanced functional coupling to IP 3 R1 channels. These pathological alterations elevate IP 3 ‐induced I Cat in arterial myocytes.