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Am J Physiol Gastrointest Liver Physiol 279: G1235-G1241, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 6, G1235-G1241, December 2000

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

Seong-Chun Kwon1,2, Hiroshi Ozaki2, and Hideaki Karaki2

1 Department of Physiology, Yonsei University College of Medicine, Seoul 120-752, Korea; and 2 Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan

In guinea pig taenia coli, the nitric oxide (NO) donor sodium nitroprusside (SNP, 1 µM) 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-clamp technique, 10 µM SNP decreased the peak Ba2+ current, and this effect was blocked by an inhibitor of soluble guanylate cyclase. Carbachol (10 µM) induced an inward current, and this effect was markedly inhibited by SNP. SNP markedly increased the depolarization-activated outward K+ currents, and this current was completely blocked by 0.3 µM iberiotoxin. SNP (1 µM) significantly increased cGMP content without changing cAMP content. Decreased Ca2+ sensitivity by SNP of contractile elements was not prominent in the permeabilized taenia, which was consistent with the [Ca2+]i-force relationship in the intact tissue. These results suggest that SNP inhibits myosin light chain phosphorylation and smooth muscle contraction stimulated by carbachol, mainly by decreasing [Ca2+]i, which resulted from the combination of the inhibition of voltage-dependent Ca2+ channels, the inhibition of nonselective cation currents, and the activation of Ca2+-activated K+ currents.

intracellular calcium concentration; calcium channel; potassium channel; nonselective cation channel; myosin light chain phosphorylation


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