Increased aortic cyclic guanosine monophosphate concentration in experimental cirrhosis in rats: Evidence for a role of nitric oxide in the pathogenesis of arterial vasodilation in cirrhosis
✍ Scribed by Michel Niederberger; Pere Ginès; Phoebe Tsai; Pierre-Yves Martin; Kenneth Morris; André Weigert; Ivan McMurtry; Robert W. Schrier
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 852 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
Arterial vasodilation is considered to be the key factor in the development of sodium and water retention leading to ascites formation in cirrhosis. To determine if nitric oxide (NO) is involved in the pathogenesis of arterial vasodilation in cirrhosis, we measured the concentration of cyclic guanosine monophosphate (cGMP), the second messenger of NO, in arterial tissue from rats with carbon tetrachlo ride-induced cirrhosis. Aortic cGMP concentration was markedly increased in cirrhotic rats, particularly in those with ascites (ascites, 826 t 70; no ascites, 597 i 48; controls, 331 2 25 fmollmg, ANOVA F = 23.1, P < .0001), and correlated inversely with arterial pressure (r = -56, P < .0001) and systemic vascular resistance (r = -.69, P = .014) and directly with cardiac index (r = .74, P < .01). The chronic administration of the NO synthesis inhibitor w-nitro-L-arginine-methylester (L-NAME) (10 mg&g/day for 7 days) induced a marked reduction in aortic cGMP concentration in cirrhotic rats with ascites to similar values obtained in L- NAME-treated control rats (86 -+ 14 vs. 89 i 8 fmoYmg, respectively, NS), indicating that the high-aortic cGMP content in cirrhotic rats was caused by an increased NO