Goldenberg K, Wergowske G, Chatterjee S, Kezdi P
Department of Medicine, Wright State University School of Medicine, Dayton, Ohio.
Clin Exp Hypertens A. 1988;10(1):91-103. doi: 10.3109/10641968809046801.
The mechanism of thiazide induced sodium and potassium transport across the cell membranes of humans has not been extensively studied. To assess the effects of thiazide diuretics on erythrocyte sodium transport and potassium distribution we measured intracellular sodium and potassium, sodium-potassium ATPase activity (with and without ouabain) and total body potassium in normokalemic and mildly hypokalemic hypertensive patients. We also measured serum and urine sodium, potassium, calcium and magnesium, plasma renin activity and serum aldosterone levels. The study patients, on long-term thiazide, had measurements obtained during, one month after cessation and one month after resumption of thiazide. In this study of normokalemic and mildly hypokalemic hypertensives there were no significant measurement changes, in contrast to previous studies of severely hypokalemic hypertensives. These results suggested that thiazide did not routinely affect erythrocyte active membrane transport and potassium distribution in the absence of severe hypokalemia.
