Renal adaptation to sodium deprivation. Effect of captopril in the rat

Dietary sodium restriction is associated with a rapid decrease in urinary sodium excretion and achievement of a new sodium balance within three to five days. In addition, renal vasoconstriction and progressive activation of intrarenal systems with vasoconstrictor (renin-angiotensin) or vasodilating (kallikrein-kinin and prostaglandins) properties are observed. The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of captopril in the rat. Treatment with captopril, before and during a six-day period after suppression of dietary sodium, was associated with sodium wasting (urinary sodium always exceeded sodium intake during the observation period); in addition, the normal increase in urinary aldosterone was blunted by about 80 percent. When captopril treatment was given for six days to rats maintained on long-term sodium restriction (at least four weeks) urinary sodium increased, although transiently; at the end of the study, renal vasodilatation together with a redistribution of glomerular blood flow to nonsuperficial glomeruli was observed. These studies indicate that captopril administration markedly blunts the renal and systemic adaptations to a reduced sodium intake in the rat. They suggest that the renin-angiotensin system is probably indispensable in preventing sodium loss when dietary sodium is suppressed.