REDUCED LIVER-FUNCTION IS THE TRIGGER FOR RENAL SODIUM RETENTION FOLLOWING PORTAL-VEIN LIGATION IN THE RAT

Sodium retention along with peripheral vasodilation are features of pr ehepatic portal hypertension. In several models of experimental liver damage, sodium retention occurs only when hepatic function, measured b y the aminopyrine breath test (ABT-k), falls below a critical threshol d. The relationship between renal sodium handling, ABT-k and systemic and renal haemodynamics in partial portal vein ligated (PVL) rats was examined to test the hypothesis that peripheral vasodilation was respo nsible for initiating sodium retention. Haemodynamic measurements were conducted early after surgery in portal hypertensive rats with and wi thout sodium retention and in sham-operated controls. Compared with co ntrol, both PVL groups of rats had elevated portal pressure and lower peripheral vascular resistance (P < 0.05). Sodium retaining-PVL rats h ad both lower ABT-k (0.95 +/- 0.05 vs 1.38 +/- 0.06 x 10(-2)/min; P < 0.05) and higher sodium balance (1.38 +/- 0.09 vs 0.43 +/- 0.09 mmol/d ay; P < 0.05) than non-sodium retaining PVL rats. No differences in pl asma renin activity or noradrenaline concentrations were observed. In a separate group of rats, hydralazine-induced peripheral vasodilation did not induce sodium retention. These results suggest that the presen ce of peripheral vasodilation alone is not sufficient to trigger a sod ium-retaining status. A factor, probably liver function-dependent, act ing directly on renal tubules may be necessary for changes in renal so dium handling in this model.