Possible Stimulation of Na+-K+-ATPase by NO Produced from Sodium Nitrite by Ultraviolet Light in Mouse Gastric Fundal Strip

Yaktubay, Naciye; Ogulener, Nuran; Önder, Serpil; Baysal, Firuz

doi:10.1016/s0306-3623(98)00067-6

Cited by 5 publications

(1 citation statement)

References 18 publications

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“…IJPs were abolished by LNA and by ODQ, indicating that NO followed by guanylate cyclase stimulation was involved in the activation of sodium pump. In other tissues, including human corpus cavernosum, NO‐induced stimulation of sodium pump activity has been reported (Gupta et al 1995; Yaktubay et al 1999). Clearly inhibition included other pathways than that resulting in the initiation of an IJP.…”

Section: Discussionmentioning

confidence: 99%

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Hashitani

2000

The Journal of Physiology

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Using intracellular recording techniques, two distinct layers of smooth muscle were identified in the rat penile bulb. The inner muscle layer (parenchyma) exhibited spontaneous action potentials, while the outer sheet (sac) was electrically quiescent. In the parenchyma, transmural stimulation initiated non‐adrenergic, non‐cholinergic (NANC) inhibitory junction potentials (IJPs) which were abolished by Nωnitro‐L‐arginine (LNA) or 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ). The amplitude of IJPs was reduced by ouabain, dinitrophenol or decreasing the extracellular potassium concentration ([K+]o) but not by several K+ channel blockers. The parenchyma also received an excitatory innervation mediated by α‐adrenoceptors which caused a contraction that was not associated with a membrane potential change. In the sac, transmural stimulation initiated two component excitatory junction potentials (EJPs) mediated by α‐adrenoceptors and associated action potentials. The initial component was more dramatically suppressed than the secondary component by caffeine, ryanodine or cyclopiazonic acid (CPA). Lowering of the extracellular chloride concentration ([Cl−]o) selectively inhibited the rapid component of EJPs, while niflumic acid was less potent. These results suggest that IJPs in the parenchyma result from the release of NO which stimulates sodium pump activity following the activation of guanylate cyclase. In the sac, the activation of α‐adrenoceptors initiates EJPs by releasing Ca2+ from intracellular stores which activates Ca2+‐activated channels.

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Section: Discussionmentioning

confidence: 99%

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Hashitani

2000

The Journal of Physiology

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Ouabain increases iNOS-dependent nitric oxide generation which contributes to the hypertrophic effect of the glycoside: possible role of peroxynitrite formation

et al. 2011

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In addition to inotropic effects, cardiac glycosides exert deleterious effects on the heart which limit their use for cardiac therapeutics. In this study, we determined the possible contribution of ouabain-induced iNOS stimulation to the resultant hypertrophic as well as cytotoxic effects of the glycoside on cultured adult rat ventricular myocytes. Myocytes were treated with ouabain (50 μM) for up to 24 h. Ouabain significantly increased gene and protein levels of inducible nitric oxide synthase (iNOS) which was associated with significantly increased release of NO from myocytes as well as increased total release of reactive oxygen species (ROS), superoxide anion (O(2) (-)), and increased peroxynitrite formation as assessed by protein tyrosine nitration. Administration of ouabain was also associated with increased levels of myocyte toxicity as determined by myocyte morphology, trypan blue staining and lactate dehydrogenase (LDH) efflux. The nonspecific NOS inhibitor Nω-nitro-L: -arginine methyl ester and the more selective iNOS inhibitor 1400W both abrogated the increase in LDH release but had no significant effect on either morphology or trypan blue staining. Ouabain also significantly increased both myocyte surface area and expression of atrial natriuretic peptide indicating a hypertrophic response with both parameters being completely prevented by NOS inhibition. The effects of iNOS inhibitors were associated with diminished ouabain tyrosine nitration as well as abrogation of ouabain-induced p38 and ERK phosphorylation. Our study shows that ouabain is a potent inducer of NO formation, iNOS upregulation, and increased production of ROS. Inhibition of ouabain-dependent peroxynitrite formation may contribute to the antihypertrophic effect of iNOS inhibition possibly by preventing downstream MAPK activation.

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Myosin light chain phosphatase activation is involved in the hydrogen sulfide-induced relaxation in mouse gastric fundus

Dhaese

Lefebvre

2009

European Journal of Pharmacology

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Possible Stimulation of Na+-K+-ATPase by NO Produced from Sodium Nitrite by Ultraviolet Light in Mouse Gastric Fundal Strip

Cited by 5 publications

References 18 publications

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Ouabain increases iNOS-dependent nitric oxide generation which contributes to the hypertrophic effect of the glycoside: possible role of peroxynitrite formation

Myosin light chain phosphatase activation is involved in the hydrogen sulfide-induced relaxation in mouse gastric fundus

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