Abstract

Vasorelaxant effects and mechanisms of the TRPV1 selective agonist capsaisin and the effect of angiotensin II on capsaicin‐induced relaxation were studied in small porcine coronary arteries (PCAs). In U46619‐constricted PCAs, capsaisin induced dose‐dependent relaxation with significant response starting at 0.1µmol/L and full relaxation at 100µmol/L. Endothelium denudation significantly inhibited relaxant responses to capsaicin at concentrations of 0.1‐10µmol/L. sPCAs pretreated with IKCa and SKCa channel blockers, TRAM‐34 and apamin, showed suppressed relaxation to capsaicin (0.1‐10µmol/L) and the inhibition was comparable to that in PCAs constricted with 40mmol/L KCl (35.5±4.7%, 29.5±3.9% vs. 79.0±4.3% in control, p<0.001). However, relaxation to 100µmol/L capsaicin remained unaffected by endothelium denudation, IKCa and SKCa blockade, or high [K+]o. Exposure of sPCAs to angiotensin II (100nmol/L) for 24h inhibited capsaicin‐induced relaxation (33.3±3.5%, p<0.001). Capsaisin induces relaxation of PCAs through both endothelium‐dependent and ‐independent mechanisms. IKCa and SKCa are involved in the endothelium‐dependent mechanism. Angiotensin II impairs capsaicin‐induced endothelium‐dependent relaxation.Supported by GRF CUHK4774/12M; NSFC 81200123; CUHK Direct Grant 4054015; Key Med. Program of Tianjin Binhai Health Bureau 2011BHKZ001; Tianjin Health Bureau 2012KZ009.Grant Funding Source: Supported by GRF CUHK4774/12M; NSFC 81200123; CUHK Direct Grant 4054015

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