ArticleThe Journal of physiology2002
Nitric oxide signalling by selective beta(2)-adrenoceptor stimulation prevents ACh-induced inhibition of beta(2)-stimulated Ca(2+) current in cat atrial myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Inhibition of L-type Ca(2+) current by ginsenoside Rd in rat ventricular myocytes.Journal of ginseng research · 2015Article
- Regulation of cardiac alternans by β-adrenergic signaling pathways.American journal of physiology. Heart and circulatory physiology · 2012Article
- Selective β2-adrenoreceptor stimulation attenuates myocardial cell death and preserves cardiac function after ischemia-reperfusion injury.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Contractile Activity Regulates Inducible Nitric Oxide Synthase Expression and NO(i) Production in Cardiomyocytes via a FAK-Dependent Signaling Pathway.Journal of signal transduction · 2012Article
- The Effects of β (2) -Adrenoreceptor Activation on the Contractility, Ca-Signals and Nitric Oxide Production in the Mouse Atria.Acta naturae · 2011Article
- Laminin enhances beta(2)-adrenergic receptor stimulation of L-type Ca(2+) current via cytosolic phospholipase A(2) signalling in cat atrial myocytes.The Journal of physiology · 2009Article
- Nonselective NOS inhibition blunts the sweat response to exercise in a warm environment.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Article
- Characteristics and function of cardiac mitochondrial nitric oxide synthase.The Journal of physiology · 2009Article
- Biphasic effect of SIN-1 is reliant upon cardiomyocyte contractile state.Free radical biology & medicine · 2008Article
- [On the function of beta3-adrenoceptors in the human heart: signal transduction, inotropic effect and therapeutic prospects].Wiener medizinische Wochenschrift (1946) · 2006Review
- Phenylephrine acts via IP3-dependent intracellular NO release to stimulate L-type Ca2+ current in cat atrial myocytes.The Journal of physiology · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The present study determined the effects of acetylcholine (ACh) on the L-type Ca(2+) current (I(Ca,L)) stimulated by beta(1)- or beta(2)-adrenergic receptor (AR) agonists in cat atrial myocytes. When isoproterenol (ISO; 0.1 microM) plus the beta(2)-AR antagonist ICI 118,551 (ISO-beta(1)-AR stimulation) or 0.1 microM fenoterol, a beta(2)-AR agonist (FEN-beta(2)-AR stimulation) increased I(Ca,L), ACh (1 microM) inhibited I(Ca,L) by -60 +/- 4 and -63 +/- 6 %, respectively. When ISO plus the beta(1)-AR antagonist atenolol (ISO-beta(2)-AR stimulation) or 1 microM zinterol (ZIN-beta(2)-AR stimulation) increased I(Ca,L), ACh-induced inhibition of I(Ca,L) was significantly smaller, at -21 +/- 3 and -24 +/- 3 %, respectively. L-N(5)-(1-iminoethyl)ornithine (L-NIO, 10 microM), an inhibitor of nitric oxide (NO) synthase, enhanced ACh-induced inhibition of I(Ca,L) when stimulated by ZIN-beta(2)-ARs, but not when stimulated by ISO-beta(1)-ARs or FEN-beta(2)-ARs. Haemoglobin (50 microM), a NO scavenger, also enhanced ACh-induced inhibition when I(Ca,L) was stimulated by ZIN-beta(2)-ARs, but not when stimulated by FEN-beta(2)-ARs. ACh-induced inhibition of I(Ca,L) stimulated by ZIN-beta(2)-ARs was not affected by 10 microM 1H-[1,2,4] oxadiazolo[4,3-a] quinoxaline-1-one (ODQ) a guanylate cyclase inhibitor, but was significantly enhanced by 500 microM reduced glutathione or 100 microM dithiothreitol, agents that act as sinks for S-nitrosylation. ACh-induced inhibition was smaller when I(Ca,L) was stimulated by spermine/NO, a NO donor, than by milrinone, a phosphodiesterase type III inhibitor. ISO (ISO-beta(1)/beta(2)-AR stimulation) increased I(Ca,L) and even though ISO releases NO, ACh prominently inhibited I(Ca,L). This inhibitory effect of ACh was enhanced by L-NIO. Stimulation of ZIN-beta(2)-ARs increased intracellular NO, whereas ISO-beta(1)-ARs or FEN-beta(2)-ARs failed to increase intracellular NO. These results indicate that in atrial myocytes, NO released by selective beta(2)-AR stimulation prevents ACh-induced inhibition of I(Ca,L) stimulated by beta(2)-ARs. NO acts via a cGMP-independent, S-nitrosylation mechanism. Although FEN acts via beta(2)-ARs, it fails to stimulate G(i)-/NO signalling and preferentially stimulates G(s)-/adenylate cyclase signalling, similar to beta(1)-ARs. These findings indicate that NO signalling modulates muscarinic receptor inhibition of atrial function stimulated by beta(2)-ARs.
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