Role of Nitric Oxide Production through M2-Cholinergic Receptors in Cultured Rat Ventricular Myocytes

1998 ◽  
Vol 251 (3) ◽  
pp. 791-795 ◽  
Author(s):  
Shuji Yamamoto ◽  
Atsushi Miyamoto ◽  
Shin Kawana ◽  
Akiyoshi Namiki ◽  
Hideyo Ohshika
Keyword(s):  
Nitric Oxide ◽  
Ventricular Myocytes ◽  
Cholinergic Receptors ◽  
Nitric Oxide Production ◽  
Rat Ventricular Myocytes ◽  
Oxide Production

Role of nitric oxide production in carbachol-induced negative chronotropy in cultured rat ventricular myocytes

1999 ◽  
Vol 366 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Shuji Yamamoto ◽  
Atsushi Miyamoto ◽  
Shin Kawana ◽  
Akiyoshi Namiki ◽  
Hideyo Ohshika
Keyword(s):  
Nitric Oxide ◽  
Ventricular Myocytes ◽  
Nitric Oxide Production ◽  
Rat Ventricular Myocytes ◽  
Oxide Production

Droperidol Inhibits Intracellular Ca2+, Myofilament Ca2+Sensitivity, and Contraction in Rat Ventricular Myocytes

2005 ◽  
Vol 102 (6) ◽  
pp. 1165-1173 ◽  
Author(s):  
Toshiya Shiga ◽  
Sandro Yong ◽  
Joseph Carino ◽  
Paul A. Murray ◽  
Derek S. Damron
Keyword(s):  
Nitric Oxide ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Nitric Oxide Production ◽  
Cellular Mechanisms ◽  
Rat Ventricular Myocytes ◽  
Oxide Production ◽  
Perfused Hearts ◽  
Ca Sensitivity

Background Droperidol has recently been associated with cardiac arrhythmias and sudden cardiac death. Changes in action potential duration seem to be the cause of the arrhythmic behavior, which can lead to alterations in intracellular free Ca concentration ([Ca]i). Because [Ca]i and myofilament Ca sensitivity are key regulators of myocardial contractility, the authors' objective was to identify whether droperidol alters [Ca]i or myofilament Ca sensitivity in rat ventricular myocytes and to identify the cellular mechanisms responsible for these effects. Methods Freshly isolated rat ventricular myocytes were obtained from adult rat hearts. Myocyte shortening, [Ca]i, nitric oxide production, intracellular pH, and action potentials were monitored in cardiomyocytes exposed to droperidol. Langendorff perfused hearts were used to assess overall cardiac function. Results Droperidol (0.03-1 mum) caused concentration-dependent decreases in peak [Ca]i and shortening. Droperidol inhibited 35 mm KCl-induced increase in [Ca]i, with little direct effect on sarcoplasmic reticulum Ca stores. Droperidol had no effect on action potential duration but caused a rightward shift in the concentration-response curve to extracellular Ca for shortening, with no concomitant effect on peak [Ca]i. Droperidol decreased pHi and increased nitric oxide production. Droperidol exerted a negative inotropic effect in Langendorff perfused hearts. Conclusion These data demonstrate that droperidol decreases cardiomyocyte function, which is mediated by a decrease in [Ca]i and a decrease in myofilament Ca sensitivity. The decrease in [Ca]i is mediated by decreased sarcolemmal Ca influx. The decrease in myofilament Ca sensitivity is likely mediated by a decrease in pHi and an increase in nitric oxide production.

Nitric oxide production by human monocytes: evidence for a role of CD23

1995 ◽  
Vol 16 (12) ◽  
pp. 574-580 ◽  
Author(s):  
Bernard Dugas ◽  
M. Djavad Mossalayi ◽  
Chantal Damais ◽  
Jean-Pierre Kolb
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Human Monocytes ◽  
Oxide Production

scholarly journals Nitric oxide-induced cardioprotection in cultured rat ventricular myocytes

2000 ◽  
Vol 278 (4) ◽  
pp. H1211-H1217 ◽  
Author(s):  
Roby D. Rakhit ◽  
Richard J. Edwards ◽  
James W. Mockridge ◽  
Anwar R. Baydoun ◽  
Amanda W. Wyatt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ventricular Myocytes ◽  
Culture Conditions ◽  
Neonatal Rat ◽  
No Donor ◽  
Rat Ventricular Myocytes ◽  
Kinase C ◽  
Neonatal Rat Ventricular Myocytes ◽  
Oxide Synthase

The aim of this study was to investigate the role of nitric oxide (NO) in a cellular model of early preconditioning (PC) in cultured neonatal rat ventricular myocytes. Cardiomyocytes “preconditioned” with 90 min of stimulated ischemia (SI) followed by 30 min reoxygenation in normal culture conditions were protected against subsequent 6 h of SI. PC was blocked by N G-monomethyl-l-arginine monoacetate but not by dexamethasone pretreatment. Inducible nitric oxide synthase (NOS) protein expression was not detected during PC ischemia. Pretreatment (90 min) with the NO donor S-nitroso- N-acetyl-l,l-penicillamine (SNAP) mimicked PC, resulting in significant protection. SNAP-triggered protection was completely abolished by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) but was unaffected by chelerythrine or the presence of glibenclamide and 5-hydroxydecanoate. With the use of RIA, SNAP treatment increased cGMP levels, which were blocked by ODQ. Hence, NO is implicated as a trigger in this model of early PC via activation of a constitutive NOS isoform. After exposure to SNAP, the mechanism of cardioprotection is cGMP dependent but independent of protein kinase C or ATP-sensitive K+ channels. This differs from the proposed mechanism of NO-induced cardioprotection in late PC.

scholarly journals 561: Role of lipid rafts in human placental nitric oxide production

2017 ◽  
Vol 216 (1) ◽  
pp. S331
Author(s):  
Gustavo Leguizamon ◽  
Cyntia Aban ◽  
Nora Martinez ◽  
Denise Trigubo ◽  
Vanesa Herlax ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lipid Rafts ◽  
Nitric Oxide Production ◽  
Oxide Production
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