Altered corticosteroid control of the erythrocyte sodium-potassium pump in the spontaneously hypertensive rat.
Recent evidence suggests that corticosteroids may participate in the regulation of erythrocyte Na,K pump activity. To examine the possible role of mineral- and glucocorticoids in the physiological control of Na,K pump in vivo, 10-week-old Sprague-Dawley (SD), Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were randomly assigned to four treatment groups (n = 10 for each): (a) sham operation, (b) bilateral adrenalectomy, (c) bilateral adrenalectomy followed by daily intraperitoneal (i.p.) injection of aldosterone, 10 micrograms/kg, (d) bilateral adrenalectomy followed by daily i.p. injections of dexamethasone 60 micrograms/kg. Fourteen days later all rats were sacrificed and the erythrocyte Na,K pump activity was assessed by two different assays: ouabain sensitive ATP hydrolysis in isolated membranes (ATPase) and 86Rb uptake by intact erythrocytes. SHR exhibited reduced Na,K pump activity as measured by ATPase (compared to WKY) and by 86Rb uptake (compared to WKY and SD rats). Adrenalectomy was associated with 22-44% reduction in ATPase in all three rat species (P less than 0.05-0.01). Adrenalectomized aldosterone or dexamethasone treated SHR, WKY and SD rats exhibited ATPase activity that was indistinguishable from the corresponding control groups. Similarly, 86Rb uptake was lower in adrenalectomized SD and WKY rats. This reduction could be at least partially prevented by daily treatment with either aldosterone or dexamethasone. In SHR adrenalectomy had no effect on 86Rb uptake whether accompanied by daily treatment with aldosterone or dexamethasone or not. These results suggest that the erythrocyte sodium potassium pump is corticosteroid dependent in normotensive rats. An abnormal response of the Na,K pump to corticosteroids is observed in SHR, with a dissociation between steroid stimulated enzymatic ATP hydrolysis and actual transmembrane pumping as measured by 86Rb uptake.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000305:Adrenal Cortex Hormones / Q000502:physiology*; D000315:Adrenalectomy; D000450:Aldosterone / Q000494:pharmacology; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007425:Intracellular Membranes / Q000378:metabolism; D007473:Ion Channels / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D011921:Rats, Inbred WKY; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
D000305:Adrenal Cortex Hormones; D007473:Ion Channels; D000450:Aldosterone; D003907:Dexamethasone; D012964:Sodium; D000251:Adenosine Triphosphatases; D012413:Rubidium; D011188:Potassium