Role of nitric oxide and prostacyclin in the control of renal perfusion in experimental cirrhosis

Authors

  • Josefa Ros,

    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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  • Joan Clària,

    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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  • Wladimiro Jiménez PhD,

    Corresponding author
    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
    • Hormonal Laboratory, Hospital Clínic i Provincial, Villarroel 170, Barcelona 08036, Spain
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  • Marta Bosch-Marcé,

    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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  • Dr Paolo Angeli,

    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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    • Dr Angeli is a visiting scientist from the Department of Clinical Medicine, University of Padova, Italy.

  • Vicente Arroyo,

    1. Liver Unit, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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  • Francisca Rivera,

    1. Hormonal Laboratory, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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  • Joan Rodés

    1. Liver Unit, Departments of Medicine and Physiology, Hospital Clínic i Provincial, University of Barcelona, Barcelona, Spain
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Abstract

Nitric oxide (NO) and prostacyclin (PGI2) are two important modulators of renal function under normal conditions; however, little is known on their contributory role in cirrhosis with ascites. In this study, mean arterial pressure, renal hemodynamics, and sodium excretion were measured in 15 rats with cirrhosis and ascites and 16 control rats. Animals were studied in normal conditions, after inhibiting the synthesis of NO (Nω-nitro-L-arginine, 50 μg ± kg−1 ± min−1) or prostaglandins (lysine acetylsalicylate, 15 mg·kg−1·min−1) and following the concomitant inhibition of both systems. Cirrhotic rats showed increased systemic pressure sensitivity and blunted renal vasoconstrictor response to nitric oxide inhibition as compared with control rats. As a consequence, the glomerular filtration rate increased in cirrhotic rats but not in control rats. In both groups of animals, NO inhibition was associated with significant increased urinary sodium and fractional sodium excretion. The only significant effect observed after prostaglandin biosynthesis inhibition was a decrease in renal plasma flow in cirrhotic rats. The concomitant inhibition of both systems reduced renal plasma flow and did not change glomerular filtration rate, with no differences between control and cirrhotic rats. Prostaglandin inhibition did not prevent the natriuretic effect of the NO inhibitor in both groups of animals. These results indicate that in experimental cirrhosis both NO and PGI2 play an important role in the maintenance of renal perfusion within normal limits. (Hepatology 1995; 22:915–920.)

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