Na-K pump activity in erythrocytes of patients with endogenous and exogenous glucocorticoid excess.
The mechanism of glucocorticoid-induced hypertension is not clarified. Recent data suggest an alteration of active electrolyte transport systems by glucocorticoids. We therefore studied the activities of the Na-K pump by measuring the Na-K-ATPase activity in erythrocyte ghosts and the ouabain-sensitive uptake of rubidium in erythrocytes of patients with Cushing's syndrome and of patients with exogenous glucocorticoid excess after treatment with fluocortolone or ACTH. Na-K-ATPase activity was significantly increased in patients with Cushing's syndrome and in patients treated with ACTH compared to the controls. Similarly, total uptake of 86Rb and the ouabain-sensitive uptake in erythrocytes were found to be above the control range both in patients with Cushing's syndrome and in patients treated with fluocortolone. There was no difference in furosemide-sensitive uptake of 86Rb. The results demonstrate an increased maximal activity of the Na-K pump in patients with glucocorticoid excess.
D000324:Adrenocorticotropic Hormone / Q000009:adverse effects; D000328:Adult; D003480:Cushing Syndrome / Q000201:enzymology*; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000201:enzymology*; D005260:Female; D005448:Fluocortolone / Q000009:adverse effects; D005938:Glucocorticoids / Q000097:blood*; D006801:Humans; D006929:Hyperaldosteronism / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood*; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood
D005938:Glucocorticoids; D005448:Fluocortolone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium