NO donor sodium nitroprusside inhibits excitation-contraction coupling in guinea pig taenia coli

In guinea pig taenia coli, the nitric oxide (NO) donor sodium nitroprusside (SNP, 1 muM) reduced the carbachol-stimulated increases in muscle force in parallel with a decrease in intracellular Ca2+ concentration ([Ca2+](i)). A decrease in the myosin light chain phosphorylation was also observed that was closely correlated with the decrease in [Ca2+](i). With the patch-clam p technique, 10 muM SNP decreased the peak Ba2+ current, and this effect wa s blocked by an inhibitor of soluble guanylate cyclase. Carbachol (10 muM) induced an inward current, and this effect was markedly inhibited by SNP. S NP markedly increased the depolarization-activated outward K+ currents, and this current was completely blocked by 0.3 muM iberiotoxin. SNP (1 muM) si gnificantly increased cGMP content without changing cAMP content. Decreased Ca2+ sensitivity by SNP of contractile elements was not prominent in the p ermeabilized taenia, which was consistent with the [Ca2+](i)-force relation ship in the intact tissue. These results suggest that SNP inhibits myosin l ight chain phosphorylation and smooth muscle contraction stimulated by carb achol, mainly by decreasing [Ca2+](i), which resulted from the combination of the inhibition of voltage-dependent Ca2+ channels, the inhibition of non selective cation currents, and the activation of Ca2+-activated K+ currents .