Abstract
The influence of dietary potassium on the natriuretic effect of hydrochlorothiazide was investigated in conscious rats which had access to 0.46 M NaCl solution; the intake of saline was used as an index of the natriuresis. Control rats drank very little saline (less than 1 mmol 24 h-1), whereas animals given hydrochlorothiazide in the food (35 mg kg-1 dry weight) increased their saline intake to approximately 10 mmol 24 h-1. In a third group of rats, on a high-potassium diet (360 mmol kg-1 dry weight vs 60 mmol kg-1 dry weight), the same dose of hydrochlorothiazide increased the saline intake to only 2 mmol 24 h-1. In order to investigate the renal mechanisms involved in these effects, animals were anaesthetized and prepared for micropuncture. Collections were made from late surface convolutions of proximal tubules and from early and late regions of distal tubules. Total glomerular filtration rate, single-nephron filtration rate, and the delivery of sodium to the end of the proximal tubule and to the beginning of the distal tubule were similar in the three groups of rats. In rats on a normal diet, hydrochlorothiazide treatment was associated with an increased delivery of sodium to the end of the distal tubule. No such increase was seen in thiazide-treated rats on a high potassium intake. It is concluded that a high potassium intake reduces the natriuretic effect of hydrochlorothiazide as a result of interference with thiazide-induced inhibition of sodium reabsorption in the distal tubule. The effect of potassium does not depend on changes in sodium handling in other nephron segments. The possible roles of aldosterone and distal tubular potassium secretion in mediating this effect are discussed.
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