Abstract
The compound BAY 41-2272 stimulates the soluble guanylyl cyclase in a nitric oxide (NO)-independent manner. We have investigated the potency and efficacy of BAY 41-2272 in the rat anococcygeus muscle, as well as the effects of BAY 41-2272 on NO-mediated anococcygeus relaxations. BAY 41-2272 (0.01–10 μM) potently relaxed precontracted anococcygeus muscle strips, with a pEC 50 value of 6.44 ± 0.03 and maximum response of 100 ± 2%. The soluble guanylyl cyclase inhibitor 1 H-[1,2,4]-oxidiazolo[4,3- a] quinoxalin-1-one (ODQ, 1 μM) and the NO inhibitor N ω-nitro- l-arginine methyl ester ( l-NAME, 100 μM) caused significant rightward shifts in the concentration–response curves to BAY 41-2272. The phosphodiesterase type-5 inhibitor tadalafil (0.1 μM) markedly enhanced the relaxations evoked by BAY 41-2272. In addition, BAY 41-2272 increased the duration of nitrergic relaxations by approximately 55%. The relaxations induced by glyceryl trinitrate were also significantly potentiated by BAY 41-2272. In conclusion, BAY 41-2272 interacts with endogenous and exogenous NO causing a potent relaxation of rat anococcygeus muscle.
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