Stimulation of soluble guanylyl cyclase by BAY 41-2272 relaxes anococcygeus muscle: Interaction with nitric oxide

Cleber E. Teixeira, Fernanda B.M. Priviero, Mário A. Claudino, Juliana S. Baracat, Gilberto De Nucci, R. Clinton Webb, Edson Antunes

Research output: Contribution to journalArticle

10 Scopus citations


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 pEC50 value of 6.44 ± 0.03 and maximum response of 100 ± 2%. The soluble guanylyl cyclase inhibitor 1H-[1,2,4]-oxidiazolo[4,3-a] quinoxalin-1-one (ODQ, 1 μM) and the NO inhibitor Nω-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.

Original languageEnglish (US)
Pages (from-to)157-165
Number of pages9
JournalEuropean Journal of Pharmacology
Issue number1-2
Publication statusPublished - Jan 13 2006



  • Anococcygeus muscle
  • BAY 41-2272
  • Nitrergic nerve
  • Nitric oxide
  • Soluble guanylyl cyclase
  • Tadalafil

ASJC Scopus subject areas

  • Pharmacology

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