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Cellular mechanisms of nitric oxide‐induced relaxation of corporeal smooth muscle in the guinea‐pig

The cellular mechanism of nitric oxide (NO)‐induced relaxation in corporeal smooth muscle (CSM) of the guinea‐pig was investigated. Changes in the intracellular concentration of calcium ions ([Ca2+]i), membrane potential and isometric tension were measured. CSM cells exhibited spontaneous depolarizations and transient increases in [Ca2+]i (Ca2+ transients) which were accompanied by contractions. This spontaneous activity was abolished by nifedipine (10 μm). NO released by 3‐morpholino‐sydnonimine (SIN‐1, 10 μm) hyperpolarized the membrane and prevented the generation of spontaneous depolarizations. SIN‐1 also abolished Ca2+ transients and associated contractions. These effects of SIN‐1 were blocked by 1H‐[1,2,4]oxadiazole[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μm), an inhibitor of guanylate cyclase. Noradrenaline (NA, 1 μm) increased [Ca2+]i to levels similar to those produced by high potassium‐containing solution (high K+ solution, [K+]o= 40 mm), however, NA‐induced contractions were three times greater in amplitude than those induced by high K+ solution. In NA precontracted preparations, SIN‐1 inhibited 80 % of the contraction and decreased [Ca2+]i by 20 %. In contrast, nifedipine reduced [Ca2+]i by 80 %, while the level of contraction was decreased by only 20 %. SIN‐1‐induced reduction in [Ca2+]i but not the tension effect, was abolished by pretreatment with cyclopiazonic acid (CPA, 10 μm). In high K+ precontracted preparations, SIN‐1 inhibited 80 % of the contraction and reduced [Ca2+]i by 20 %. Nifedipine, however, largely abolished increases in both [Ca2+]i and tension under these circumstances. These results suggest that decreasing the sensitivity of contractile proteins to Ca2+ is probably the key mechanism of NO‐induced relaxation in CSM of the guinea‐pig.