Abstract
SummarySodium deficiency and salt overload failed to influence degree of proteinuria and biochemical and ultrastructural features of AN nephrosis. Ascites was absent in AN-treated, sodium deficient rats which exhibited elevated JGI and increased width of zona glomerulosa (ZGI) of adrenal cortex; whereas AN-treated rats subjected to salt overload had massive ascites but normal JGI and ZGI. This information indicates that the elevated JGI and ZGI observed in AN-treated rats maintained with a normal sodium-containing diet are not due to ascites per se. Although the changes encountered in this study in JGI may be due to alteration in blood volume, emphasis is also directed to the causal effects of electrolyte alterations and blood osmolarity. Parallel changes of JGI and ZGI are interpreted as evidence of activity of the renin-angiotensin-aldosterone mechanism in AN nephrosis and the secondary role of aldosterone in ascites production in this syndrome.
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Schedule a callMore From: Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
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