Hyperaldosteronism in the sodium-depleted rat: mode of aldosterone-stimulating action of frusemide.
The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin-angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.
D000311:Adrenal Glands / Q000187:drug effects / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology*; D006929:Hyperaldosteronism / Q000378:metabolism / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012083:Renin / Q000097:blood; D012636:Secretory Rate / Q000187:drug effects; D012964:Sodium / Q000172:deficiency*; D013268:Stimulation, Chemical; D013722:Teprotide / Q000494:pharmacology
D000450:Aldosterone; D005665:Furosemide; D003907:Dexamethasone; D012964:Sodium; D013722:Teprotide; D012083:Renin; D011188:Potassium; D007213:Indomethacin