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Role of Transient Receptor Potential (TRP) Channels in Cyclic ADP‐Ribose (cADPR)‐Mediated Sex‐Differences in Agonist‐Induced Contraction of Rat Aorta
Author(s) -
Guedes Alonso G.P.,
Stallone John N.
Publication year - 2010
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.24.1_supplement.1041.6
Subject(s) - contraction (grammar) , chemistry , phenylephrine , endocrinology , medicine , antagonist , agonist , ergometrine , transient receptor potential channel , vasoconstriction , aorta , cyclic adp ribose , receptor , biology , biochemistry , genetics , cd38 , stem cell , cd34 , blood pressure
cADPR signaling is emerging as a significant mechanism underlying sex differences in agonist‐induced vasoconstriction. Here we investigated the role of TRP‐channels in cADPR‐mediated sex differences in vasopressin (VP)‐ and phenylephrine (PE)‐induced contraction of male (M) and female (F) rat aorta. Isometric tension was measured in endothelium‐denuded aortic rings from age‐matched, sex intact, M and F SD rats (n=6–10/group). Maximal responses (mean ± SE) to VP in M (3.3 ± 0.2 g/mg dry tissue) and F (4.1 ± 0.2), respectively, decreased by 53% (1.5 ± 0.3) and 0.1% (4.0 ± 0.3) with cADPR antagonist 8‐Br‐cADPR (8‐Br; 30 μM); by 56% (1.4 ± 0.1) and 39% (2.4 ± 0.4) with TRP‐channel antagonist SKF‐96365 (SKF; 15 μM); and by 64% (1.2 ± 0.3) and 53% (1.7 ± 0.3) with both 8‐Br and SKF. Maximal responses to PE in M (4.2 ± 0.2) and F (3.9 ± 0.2), respectively, decreased by 16% (3.5 ± 0.1) and 26% (2.9 ± 0.3) with 8‐Br; by 38% (2.6 ± 0.2) and 33% (2.6 ± 0.2) with SKF; and by 59% (1.7 ± 0.3) and 51% (1.9 ± 0.4) with both 8‐Br and SKF. Thus, the cADPR contribution to VP‐induced contraction in M is markedly TRP channel‐dependent. VP‐induced contraction of F aorta is noticeably less dependent on TRP‐channels and almost entirely cADPR‐independent. cADPR contribution to PE‐induced contraction appears to be independent of TRP channels in both M and F. Hence, the role of TRP‐channels in cADPR‐dependent contraction of rat aorta is both agonist‐ and sex‐specific.