Dual nitric oxide mechanisms of cholestasis-induced bradycardia in the rat.

Abstract:

:1. Cholestatic liver disease is associated with nitric oxide (NO) overproduction and bradycardia. Nitric oxide has a dual effect on sinoatrial node and its effects depend on its concentration. Nitric oxide can increase heart rate by activating hyperpolarization-activated pacemaker current (If) but, at high concentrations, it can potentially decrease heart rate by inhibition of L-type calcium current. In the present study, the responsiveness of isolated atria to CsCl (an inhibitor of the If current) and acetylcholine (ACh; which decreases L-type calcium current through a NO-dependent pathway) were evaluated in bile duct-ligated and sham-operated control rats. 2. Bile duct ligation induced a significant decrease in the negative chronotropic effect of CsCl (0.2-5 mmol/L), but increased the responsiveness of isolated atria to ACh (10-8 to 10-3 mol/L). These effects were restored after incubation of the atria in the presence of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (0.1 mmol/L). 3. Anaesthetized bile duct-ligated rats showed bradycardia and the plasma levels of NO2-/NO3- were significantly higher in bile duct-ligated rats compared with sham-operated animals. 4. Different and opposite responses of atria of cholestatic rats to CsCl and ACh can be explained by NO overproduction in bile duct-ligated animals. A dual role of NO in the regulation of the sinoatrial node may be responsible for this opposite effect and may have a role in the pathophysiology of cholestasis-induced bradycardia.

authors

Mani AR,Nahavandi A,Moosavi M,Safarinejad R,Dehpour AR

doi

10.1046/j.1440-1681.2002.03748.x

keywords:

subject

Has Abstract

pub_date

2002-10-01 00:00:00

pages

905-8

issue

10

eissn

0305-1870

issn

1440-1681

pii

3748

journal_volume

29

pub_type

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