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The present study examined the role of the soluble guanylyl cyclase in the control of basal activity of the K<jats:sub>Ca<\/jats:sub>channels and in mediating NO-induced activation of the K<jats:sub>Ca<\/jats:sub>channels in vascular smooth muscle cells, using a selective inhibitor of this enzyme, 1<jats:italic>H<\/jats:italic>-[1,2,4]oxadiazolo[4,2-\u03b1]quinoxalin-1-one (ODQ). In the cell-attached patch-clamp mode, addition of ODQ into the bath solution (10 \u03bcmol\/L) decreased the K<jats:sub>Ca<\/jats:sub>channel activity by 59% and attenuated activation of the channels induced by the NO donor, deta nonoate, by 70%. ODQ had no effect on 8-bromo-cGMP-induced activation of the K<jats:sub>Ca<\/jats:sub>channels. Deta nonoate produced a concentration-dependent relaxation of precontracted coronary arteries. When ODQ was added to the bath, the deta nonoate-induced relaxations were inhibited. The IC<jats:sub>50<\/jats:sub>for deta nonoate was decreased by about 25-fold and the maximal effect of deta nonoate was reduced by about 60%. A specific K<jats:sub>Ca<\/jats:sub>channel inhibitor, iberiotoxin, decreased deta nonoate-induced vasodilation but to a lesser extent than ODQ. However, ODQ was without effect on the vasodilation induced by a prostacyclin analog, iloprost, and by adenosine. These results indicate that a soluble guanylyl cyclase and cGMP play an important role in the control of the K<jats:sub>Ca<\/jats:sub>channel activity in coronary arterial smooth muscle cells. K<jats:sub>Ca<\/jats:sub>channel activation participates in the NO-induced vasodilation in coronary circulation.<\/jats:p>","DOI":"10.1161\/01.hyp.31.1.303","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"303-308","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":42,"title":["Effect of Selective Inhibition of Soluble Guanylyl Cyclase on the K<sub>Ca<\/sub>Channel Activity in Coronary Artery Smooth Muscle"],"prefix":"10.1161","volume":"31","author":[{"given":"Pin-Lan","family":"Li","sequence":"first","affiliation":[{"name":"From the Departments of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wis."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Man-Wen","family":"Jin","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wis."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William B.","family":"Campbell","sequence":"additional","affiliation":[{"name":"From the Departments of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wis."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/327524a0"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/368850a0"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.4.C799"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.1.C299"},{"key":"e_1_3_2_5_2","first-page":"167","volume":"463","year":"1993","unstructured":"Taniguchi J, Furukawa KI, Shigekawa M. 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