[Mechanisms underlying rat coronary arterial vasoconstriction induced by blockade of inward rectifier potassium channels with BaCl 2 ].

In order to explore the mechanisms underlying the vasoconstriction induced by blockade of inward rectifier K channels (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 Ca deprivation 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 BaCl in Ca-free solution and by followed restoration of 2.5 mmol/L Ca accounted 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 BaCl induces 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.