Nitric Oxide Synthase/Guanylate Cyclase Pathway Modulates the Rat Vas Deferens Contractility Induced by Phenylephrine

Abstract: The involvement of the nitric oxide synthase/soluble guanylate cyclase pathway on the modulation of phenylephrine‐induced contractility in the rat vas deferens was investigated. Phenlylephrine‐concentration response curves were obtained in absence and in presence of inhibitors, NG‐Nitro‐L‐arginine (L‐NOARG), NG‐Nitro‐L‐arginine methyl esther (L‐NAME) or NG‐monomethyl‐L‐arginine (L‐NMMA) or GC inhibitior, 1H‐(1,2,4)‐oxadiaziol‐(4,3‐a)quinoxalin‐1‐one (ODQ) or nitric oxide donor, 3‐morpholinosydnonimine hydrochloride (SIN‐1) alone or together with L‐NMMA or ODQ. Both nitric oxide synthase and GC inhibitors reduced the Phe‐Emax. SIN‐1 alone did not change phenylephrine‐induced responses and it could reverse the L‐NMMA effect but not ODQ effect. The reduction of the phenylephrine‐induced contractility obtained in consequence of the inhibition of the nitric oxide/GC pathway suggest that, in the rat vas deferens, despite its well identified relaxant properties, nitric oxide potentiates the contractility induced by adrenergic stimulation.