Corticoid effects on angiotensin- and norepinephrine-induced proteinuria in rats.
Adrenalectomy is known to prevent the proteinuria induced by renin or angiotensin, but it is not clear whether the loss of glucocorticoids or mineralocorticoids is responsible. The problem was reinvestigated using dexamethasone and aldosterone, essentially pure glucocorticoid and mineralocorticoid, respectively. Dexamethasone treatment for 2--5 days completely restored the protein-uric response to angiotensin II or norepinephrine, but aldosterone did not, even though the dose and treatment were sufficient to induce changes in electrolyte excretion. Fractional sodium excretion was also increased by angiotensin II and norepinephrine in the dexamethasone-treated rats, but not in the aldosterone-treated rats. Both dexamethasone and aldosterone treatments restored the increase in filtration fraction, but the increase was not associated with proteinuria in some groups, and it is concluded that there is no causal relationship between increased filtration fraction and proteinuria. Reasons for considering binding of norepinephrine and angiotensin to the glomerular basement membrane as causal for the proteinuria and the hormonal requirements for such binding are discussed.
D000450:Aldosterone / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D007444:Inulin / Q000652:urine; D009638:Norepinephrine / Q000494:pharmacology*; D011507:Proteinuria / Q000139:chemically induced* / Q000652:urine; D051381:Rats; D012964:Sodium / Q000652:urine; D010130:p-Aminohippuric Acid / Q000652:urine
D000804:Angiotensin II; D000450:Aldosterone; D003907:Dexamethasone; D007444:Inulin; D012964:Sodium; D009638:Norepinephrine; D010130:p-Aminohippuric Acid