RESUMO
In order to explore the mechanisms underlying the vasoconstriction induced by blockade of inward rectifier Kchannels (K) with BaCl, myogenic tone of isolated rat coronary artery (RCA) was recorded with wire myograph. The dependence of BaCl- induced contraction on intracellular Ca([Ca]) release and extracellular Ca([Ca]) influx was studied by Cadeprivation and restoration. The mechanisms underlying BaCl-induced RCA contraction were investigated with specific inhibitors. BaCl(0.1-1.0 mmol/L) contracted isolated RCA in a concentration-dependent manner and the maximal contraction was (5.69 ± 1.07) mN, nearly equal to contraction induced by 60 mmol/L KCl. The contractions induced by BaClin Ca-free solution and by followed restoration of 2.5 mmol/L Caaccounted for (35.44 ± 6.72)% and (64.56 ± 5.94)%, respectively. Calcium channel blocker nifedipine (0.3 μmol/L), cyclooxygenase inhibitor indomethacin (100 μmol/L), ERK1/2 inhibitor PD98059 (10 μmol/L) and chloride channel blocker niflumic acid (100 μmol/L) pretreatment depressed the BaCl-induced maximal contraction by (87.82 ± 5.43)% (P < 0.01), (73.23 ± 5.47)% (P < 0.01), (75.69 ± 7.94)% (P < 0.01) and (83.24 ± 7.69)% (P < 0.01), respectively. These results demonstrate that BaClinduces vasoconstriction in RCA by enhancing both [Ca]release and [Ca]influx, and suggest that increase of prostanoids synthesis, activation of calcium channels and chloride channels, as well as ERK1/2 pathway may be involved in this process.