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Am J Physiol Gastrointest Liver Physiol 265: G1045-G1049, 1993;
0193-1857/93 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 265, Issue 6 1045-G1049, Copyright © 1993 by American Physiological Society

ARTICLES

Pressure diuresis and natriuresis in cirrhotic rats

N. M. Atucha, M. Cegarra, A. Ramirez, T. Quesada and J. Garcia-Estan
Departamento de Fisiologia, Facultad de Medicina, Murcia, Spain.

Arterial hypotension in liver cirrhosis has been proposed as a major mechanism contributing to renal sodium and water retention. To evaluate kidney excretory responses at different levels of arterial pressure (AP), we have characterized the relationships between renal perfusion pressure (RPP) and sodium and water excretion in carbon tetrachloride cirrhotic rats. Experiments were performed in anesthetized control (n = 9) and cirrhotic rats with (Asc, n = 6) and without ascites (Cir, n = 6) by mechanically adjusting vascular resistance in animals with renal denervation and infused with main systemic hormones. Control and Cir animals showed similar glomerular filtration rates (GFR), renal blood flows, hematocrits (Hct), and plasma proteins (PP). However, Hct, PP, and GFR were significantly lower in the Asc rats. For the same level of RPP, both cirrhotic groups excreted significantly less water and sodium than controls. Then, the pressure diuresis and natriuresis relationships of the Cir animals were significantly depressed, but those of the Asc animals were more reduced than those of the Cir rats. These results indicate that the cirrhotic kidney is not able to normally increase the sodium and water excretion in response to changes in AP. Intrarenal mechanisms, and not mainly RPP, are likely mediators of the renal alterations of liver cirrhosis.


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