The role of nitric oxide in bradycardia of rats with obstructive cholestasis

Nahavandi, Arezo; Dehpour, Ahmad Reza; Mani, Ali R.; Homayounfar, Homayoun; Abdoli, Ali; Abdolhoseini, Mohammad Reza

doi:10.1016/s0014-2999(00)00773-1

Cited by 36 publications

(46 citation statements)

References 31 publications

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“…28 Rats with biliary cirrhosis are bradycardic, 29 and this condition is owing to a significant hyporesponsiveness to the chronotropic effect of catecholamines. 7,8 In the present study, we showed that two independent treatments (N-acetylcysteine and L-NAME), both of which can normalize chronotropic responses to adrenergic stimulation in vitro, also led to normalization of heart rate in vivo (Fig. 2).…”

Section: Discussionsupporting

confidence: 60%

“…Similarly, we have shown that increased NO synthesis in bile ductligated (BDL) rats causes bradycardia by causing impaired responsiveness of cardiac pacemaker cells to adrenergic stimuli. 7,8 Nitric oxide is involved in the modulation of cardiac function in the normal heart, as well as in various cardiac diseases via mechanisms involving NO that are both dependent on and independent of guanylyl cy-clase. 9,10 For example, evidence suggests NO attenuates cardiac pacemaker activity, mediated by cyclic guanosine monophosphate (cGMP).…”

mentioning

confidence: 99%

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Nitration of cardiac proteins is associated with abnormal cardiac chronotropic responses in rats with biliary cirrhosis†

et al. 2006

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Acceleration of the heart rate in response to catecholamines is impaired in cirrhosis. In this study, we tested the hypothesis that increased formation of reactive nitrogen species in biliary cirrhosis causes nitration of cardiac proteins and leads to impaired chronotropic function. Bile duct-ligated (rats with cirrhosis) or sham-operated rats were injected daily with either saline, N G -L-nitro-arginine methyl ester (L-NAME), or N-acetylcysteine for 7 days from week 3 to week 4 after surgery. Cardiac chronotropic responsiveness to ␤-adrenergic stimulation was assessed in vitro using spontaneous beating isolated atria. Nitration of cardiac proteins was measured by mass spectrometry and located by immunogold electron microscopy. Marked impairment of chronotropic responses of isolated atria to isoproterenol was seen in rats with cirrhosis, which normalized after the administration of N-acetylcysteine or L-NAME. The levels of protein-bound nitrotyrosine in atrial tissue increased from 16 ؎ 1 to 23 ؎ 3 pg/g tyrosine in rats with cirrhosis, and decreased to 15 ؎ 1 and 17 ؎ 1 pg/g after treatment with L-NAME and N-acetylcysteine, respectively (P < .05). Immunogold electron microscopy demonstrated increased nitration of mitochondrial proteins in the atria of rats with cirrhosis. The plasma nitrite/nitrate levels were elevated in rats with biliary cirrhosis, and decreased after administration of L-NAME but were unchanged by N-acetylcysteine. In conclusion, abnormal cardiac chronotropic function in cirrhosis is associated with increased nitration of cardiac proteins. Two independent treatments (N-acetylcysteine and L-NAME) that decrease nitration of cardiac proteins led to normalization of cardiac responses. Nitration of critical proteins in cardiac tissue may lead to abnormal cardiac function. (HEPATOLOGY 2006;43:847-856.)

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Section: Discussionsupporting

confidence: 60%

mentioning

confidence: 99%

Nitration of cardiac proteins is associated with abnormal cardiac chronotropic responses in rats with biliary cirrhosis†

et al. 2006

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“…These marked sinusoidal dilatation due to NO vasodilatation effect [68] indicating the enhancing effect of l-arginine on anti-hepato-toxicity activities of Sly. In harmony with our results, Nahavandi et al was found that histo-pathological changes were partially but significantly prevented by exogenous larginine in obstructive jaundiced rats where l-arginine played a protective role by inducing iNOS expression and NO synthesis [69]. Tables Figure 1: Effect of administration of silymarin (100mg/kg), l-arginine (200mg/kg) and their combination on ALT enzyme activity in cisplatin-induced liver toxicity in normally fed and in protein malnourished rats.…”

Section: Influence Of L-arginine On Cisplatin-induced Hepatotoxicity supporting

confidence: 92%

“…Endothelial nitric oxide synthase (eNOs) produces nitric oxide (NO) from l-arginine. NO can rapidly react with reactive oxygen species to form peroxynitrite which generally relief the oxidative stress (antioxidants) [69]. Although, l-arginine is synthesized in the body, it is not produced in sufficient quantities to support growth or meet metabolic requirements during the periods of PM [27].…”

Section: Introductionmentioning

confidence: 99%

Influence of L-arginine on Cisplatin-Induced Hepatotoxicity in both normally Fed and Protein Malnourished Rats

El-Hamid¹,

Ali²,

Ahmed³

et al. 2016

IOSR

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“…The production of hepatocytic nitric oxide found to be markedly increased in obstructive jaundice in multiple studies conducted on rats hearts (12,13). Overall, these results suggest a negative regulatory effect of NO on cardiac myocytes in obstructive jaundice (8,14).…”

Section: Discussion:-mentioning

confidence: 70%

Obstructive Jaundice- Induced Sinus Bradycardia in Child With Sickle Cell Disease.

Almadani¹,

Alansari²,

Alsaied.³

2017

IJAR

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The role of nitric oxide in bradycardia of rats with obstructive cholestasis

Cited by 36 publications

References 31 publications

Nitration of cardiac proteins is associated with abnormal cardiac chronotropic responses in rats with biliary cirrhosis†

Nitration of cardiac proteins is associated with abnormal cardiac chronotropic responses in rats with biliary cirrhosis†

Influence of L-arginine on Cisplatin-Induced Hepatotoxicity in both normally Fed and Protein Malnourished Rats

Obstructive Jaundice- Induced Sinus Bradycardia in Child With Sickle Cell Disease.

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