PMID: 8584047Sep 1, 1995Paper

Evidence against a role of nitric oxide in the indirect negative inotropic-effect of M-cholinoceptor stimulation in human ventricular myocardium

Naunyn-Schmiedeberg's Archives of Pharmacology
H KilterM Böhm

Abstract

Nitric oxide (NO) has been reported to mediate several effects in response to muscarinic cholinergic stimulation in cardiovascular tissues. Recently, an attenuation of guinea pig cardiac myocyte contraction by NO has been described. The aim of the present study was to determine whether the indirect negative inotropic effect of M-cholinoceptor stimulation in human myocardium is in part due to an effect of endogenous NO. Therefore, the effect of carbachol was studied under control conditions and during inhibition of NO-synthase by pretreatment with NG-monomethyl-L-arginine (NMMA). Functional experiments were performed in isolated, electrically driven (1 Hz, 37 degrees C) left ventricular papillary muscle strips of human myocardium. Since cytokines have been reported to be increased in the serum of patients with heart failure and could induce NO-synthase activity in failing myocardium, we compared samples from nonfailing and terminally failing (classified as NYHA IV) hearts. The indirect negative inotropic effect of carbachol (10 mumol/l) was studied in the presence of the beta-adrenoceptor agonist isoprenaline (0.03 mumol/l). After stimulation with isoprenaline, carbachol significantly (P < 0.05) reduced force of contraction. Thi...Continue Reading

Citations

Apr 13, 2000·Pharmacology & Therapeutics·A M Shah, P A MacCarthy
Aug 13, 2004·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Claire E SearsBarbara Casadei
Sep 1, 2001·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·S DheinO E Brodde

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