Hyperaldosteronism in the sodium-depleted rat: mechanism of aldosterone stimulation by peritoneal dialysis with glucose solution.
Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.
D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D006929:Hyperaldosteronism / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D010530:Peritoneal Dialysis; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012083:Renin / Q000097:blood; D012636:Secretory Rate / Q000187:drug effects; D012964:Sodium / Q000172:deficiency* / Q000378:metabolism; D013268:Stimulation, Chemical
D000450:Aldosterone; D003907:Dexamethasone; D012964:Sodium; D012083:Renin; D005947:Glucose; D011188:Potassium