{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T15:48:12Z","timestamp":1761580092736},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2003,1,1]],"date-time":"2003-01-01T00:00:00Z","timestamp":1041379200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2003,1]]},"abstract":"<jats:p>In the guinea pig gastric antrum, the effects of sodium nitroprusside (SNP), an NO donor, on pacemaker potentials were investigated in the presence of nifedipine. The pacemaker potentials consisted of primary and plateau components; SNP (&gt; 1 \u03bc<jats:sc>m<\/jats:sc>) increased the frequency of occurrence of these pacemaker potentials, while inhibiting the plateau component. 1<jats:italic>H<\/jats:italic>\u2010[1,2,4]\u2010Oxadiazole [4,3\u2010a] quinoxalin\u20101\u2010one, an inhibitor of guanylate cyclase, had no effect on the excitatory actions of SNP on the frequency of pacemaker potentials. Other types of NO donor, (\u00b1)\u2010<jats:italic>S<\/jats:italic>\u2010nitroso\u2010<jats:italic>N<\/jats:italic>\u2010acetylpenicillamine, 3\u2010morpholino\u2010sydnonimine and 8\u2010bromoguanosine 3\u20325\u2019\u2010cyclic monophosphate had no excitatory effect on pacemaker activity. Forskolin, an activator of adenylate cyclase, or 4,4\u2032\u2010diisothiocyano\u2010stilbene\u20102,2\u2032\u2010disulphonic acid, an inhibitor of the Ca<jats:sup>2+<\/jats:sup>\u2010activated <jats:styled-content>Cl<jats:sup>\u2212<\/jats:sup><\/jats:styled-content> channel, strongly attenuated the generation of pacemaker potentials, and SNP added in the presence of these chemicals restored the generation of pacemaker potentials. The pacemaker potentials evoked by SNP were abolished in low\u2010Ca<jats:sup>2+<\/jats:sup> solution or by membrane depolarization with high\u2010K<jats:sup>+<\/jats:sup> solution. The SNP\u2010induced generation of pacemaker potentials was not prevented by cyclopiazonic acid, an inhibitor of internal Ca<jats:sup>2+<\/jats:sup>\u2010ATPase, but was limited to a transient burst by iodoacetic acid, an inhibitor of glycolysis, carbonyl cyanide <jats:italic>m<\/jats:italic>\u2010chlorophenyl\u2010hydrazone, a mitochondrial protonophore, or 1,2\u2010bis(2\u2010aminophenoxy)ethane\u2010<jats:italic>N,N,N<\/jats:italic>\u2018,<jats:italic>N<\/jats:italic>\u2018\u2010tetraacetic acid acetoxymethyl ester, an intracellular Ca<jats:sup>2+<\/jats:sup> chelator. These results suggest that the SNP\u2010induced increase in the frequency of pacemaker potentials is related to the elevated intracellular Ca<jats:sup>2+<\/jats:sup> concentrations due to release from mitochondria, and these actions may be independent of the activation of guanylate cyclase.<\/jats:p>","DOI":"10.1113\/jphysiol.2002.027607","type":"journal-article","created":{"date-parts":[[2003,1,1]],"date-time":"2003-01-01T03:57:03Z","timestamp":1041393423000},"page":"191-205","source":"Crossref","is-referenced-by-count":18,"title":["Pacemaker frequency is increased by sodium nitroprusside in the guinea pig gastric 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