Nitric oxide synthase-containing neurones and nerve fibres within cardiac ganglia of rat and guinea-pig: an electron-microscopic immunocytochemical study

Sosunov, Alexander A.; Hassall, C. J. S.; Loesch, Andrzej; Turmaine, Mark; Burnstock, Geoffrey

doi:10.1007/s004410050563

Cited by 39 publications

(24 citation statements)

References 28 publications

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“…Our findings agree with previous data [12,14] on the existence of species-specific peculiarities or cellcell communication mediated by NO and on Ihe ambiguity of NO effect on cells, in pro-titular under pathological conditions.…”

Section: Resultssupporting

confidence: 95%

Effect of NO-synthase inhibitor L-NAME on occlusion and reperfusion arrhythmias in cats

et al. 1999

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On the model of occlusion/reperfusion arrhythmia in cats it was shown that repeated injections of the NO-synthase inhibitor L-NAME decreased the incidence of occlusion arrhythmias (to 40%), eliminated reperfusion-induced ventricular fibrillation, and drastically reduced the latency of occlusion arrhythmias. A single injection of L-NAME (20 mg/kg) immediately before ligation of the coronary artery did not decrease the incidence of occlusion and reperfusion arrhythmias. Key Words: ventricular arrhythmias; nitric oxide; NO-synthase inhibitorNitric oxide (NO) is an intercellular transmitter, which affects various cell processes by modulating activity of metal-containing enzymes and formation of oxygen radicals [4]. NO is produced during conversion of arginine into citrulline catalyzed by constitutive and inducible isolbrms of NO-synthase (NOS). NO plays an important role in the ischemic pathology of the myocardium. There are experimental data on both protective and cytotoxic effects of NO [6,13]. The role of NO in the genesis of ischemia/reperfusion disturbances of the cardiac rhythm remains unclear, and experimental data are in many respects controversial [9,10,12,13].Our aim was to study the effect of a nonspecific inhibitor of NOS, N0~-nitro-L-arginine methyl ester (L-NAME) on the development of occlusion and reperfusion arrhythmias in cats. MATERIALS AND METHODSExperiments were carried out on 38 mature cats of both sexes weighing 2.5-3.5 kg. The descending branch of the left coronary artery was ligated for 30 min under Department of Faculty Therapy, Department of Cytology, Histology, and Embryology, N. P. Ogarev Mordovian State University, Saransk hexenal narcosis (40 mg/kg) and then the ligature was removed and perfusion was restored.In the present study we used L-NAME (Sigma), a non-specific inhibitor of NOS, which blocks the constitutive and inducible isotorms of this enzyme. In series I (n=5), L-NAME (20 mg/kg) was infused 10 min prior to applying the ligature. In series II (n=5), the inhibitor was injected intraperitoneally during 3 days (10 mg/kg/day) and intravenously on the 4th day (20 mg/kg) immediately before coronary occlusion.The control cats were injected with 0.9% NaCI. ECG was recorded during occlusion and 20 min of reperfusion. The data were statistically analyzed using the ~2 test. RESULTSIn the control series, ventricular extrasystole and tachycardia developed in all cats after ligating of coronary artery, in some cats fatal ventricular fibrillation was observed. When the coronary blood flow was restored, reperfusion arrhythmias appeared in 100% cals, and ventricular fibrillation in 65% cats (Table 1).Single injection of L-NAME immediately before ligation of the coronary artery did not change the incidence of arrhythmias and ventricular fibrillation during both during ischemia and reperfusion, which were 0007-4888/99/0005-0460522.00 e1999 Kluwer Academic/Plemml Publisllers

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Section: Resultssupporting

confidence: 95%

Effect of NO-synthase inhibitor L-NAME on occlusion and reperfusion arrhythmias in cats

et al. 1999

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“…A similar mechanism may be present in cardiac ganglia. Sosunov et al have shown by immunocytochemical analysis that neurons within cardiac ganglia of the rat and guinea pig contain NOS (38). They further argue, Figure 4.…”

Section: Discussionmentioning

confidence: 94%

Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.

Jumrussirikul¹,

Dinerman²,

Dawson³

et al. 1998

J. Clin. Invest.

114

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Nitric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholinergic control of heart rate (HR). However, it is not known whether NO synthesized within neurons plays a role in HR regulation. HR dynamics were measured in 24 wild-type (WT) mice and 24 mice in which the gene for neuronal NO synthase (nNOS) was absent (nNOS Ϫ / Ϫ mice). Mean HR and HR variability were compared in subsets of these animals at baseline, after parasympathetic blockade with atropine (0.5 mg/kg i.p.), after ␤ -adrenergic blockade with propranolol (1 mg/kg i.p.), and after combined autonomic blockade. Other animals underwent pressor challenge with phenylephrine (3 mg/kg i.p.) after ␤ -adrenergic blockade to test for a baroreflex-mediated cardioinhibitory response. The latter experiments were then repeated after inactivation of inhibitory G proteins with pertussis toxin (PTX) (30 g/kg i.p.). At baseline, nNOS Ϫ / Ϫ mice had higher mean HR (711 Ϯ 8 vs. 650 Ϯ 8 bpm, P ϭ 0.0004) and lower HR variance (424 Ϯ 70 vs. 1,112 Ϯ 174 bpm 2 , P ϭ 0.001) compared with WT mice. In nNOS Ϫ / Ϫ mice, atropine administration led to a much smaller change in mean HR ( Ϫ 2 Ϯ 9 vs. 49 Ϯ 5 bpm, P ϭ 0.0008) and in HR variance (64 Ϯ 24 vs. Ϫ 903 Ϯ 295 bpm 2 , P ϭ 0.02) than in WT mice. In contrast, propranolol administration and combined autonomic blockade led to similar changes in mean HR between the two groups. After ␤ -adrenergic blockade, phenylephrine injection elicited a fall in mean HR and rise in HR variance in WT mice that was partially attenuated after treatment with PTX. The response to pressor challenge in nNOS Ϫ / Ϫ mice before PTX administration was similar to that in WT mice. However, PTX-treated nNOS Ϫ / Ϫ mice had a dramatically attenuated response to phenylephrine. These findings suggest that the absence of nNOS activity leads to reduced baseline parasympathetic tone, but does not prevent baroreflex-mediated cardioinhibition unless inhibitory G proteins are also inactivated. Thus, neuronally derived NO and cardiac inhibitory G protein activity serve as parallel pathways to mediate autonomic slowing of heart rate in the mouse. ( J. Clin. Invest.

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“…It is likely that the basal fluorescence signal could originate from a number of sources since NO synthases can be found in endothelial cells (Miethke et al, 2003), neurones and nerve fibres of cardiac ganglia (Sosunov et al, 1996;Sosunov et al, 1995) and subcellularly located within cardiac myocytes e.g. sarcoplasmic reticulum and mitochondria (Xu et , 1999;Kanai et al, 2001).…”

Section: Origins Of Basal No Signalmentioning

confidence: 99%

A novel method of measuring nitric-oxide-dependent fluorescence using 4,5-diaminofluorescein (DAF-2) in the isolated Langendorff-perfused rabbit heart

Patel

Brack

Coote

et al. 2008

Pflugers Arch - Eur J Physiol

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4,5-diaminofluorescein (DAF-2) has been used to measure nitric oxide (NO) activity from a variety of preparations. The aim of this study was to develop a method to assess changes in NO fluorescence using DAF-2 in isolated rabbit hearts (2.0-2.5kg:n=8). Hearts were perfused in constant flow Langendorff mode and instrumented to record aortic perfusion pressure, left ventricular pressure and left ventricular epicardial fluorescence using a bifurcated light guide at excitation wavelengths of 470±10nm, 480±10nm, 490±10nm and 500±10nm collected at 535nm. DAF-2 DA was loaded using a single bolus 150μl (1μmol) injection. Changes in NOdependent fluorescence were determined using the NO donor sodium nitroprusside Our data suggests that DAF-2 DA is a useful fluorescence indicator for measuring NO activity in isolated hearts.

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Nitric oxide synthase-containing neurones and nerve fibres within cardiac ganglia of rat and guinea-pig: an electron-microscopic immunocytochemical study

Cited by 39 publications

References 28 publications

Effect of NO-synthase inhibitor L-NAME on occlusion and reperfusion arrhythmias in cats

Effect of NO-synthase inhibitor L-NAME on occlusion and reperfusion arrhythmias in cats

Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.

A novel method of measuring nitric-oxide-dependent fluorescence using 4,5-diaminofluorescein (DAF-2) in the isolated Langendorff-perfused rabbit heart

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