Suppression of renin release by intravascular volume expansion during chronic diuretic treatment

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Circulating renin is influenced by many factors. In the clinical setting, alterations in body water and sodium balance influence plasma renin activity (PRA) significantly. Thus, with dietary sodium deprivation,1–3 rapid diuresis with furose-mide,4 and water deprivation5 PRA increases as it does also in association with the modest oligemia that accompanies long-term hydrochlorothiazide or spironolactone treatment of hypertension.6, 7 Conversely, lowered PRA has been observed following high sodium diet,1, 3 overhydration,3 in primary aldosteronism,8, 9 and following rapid intravascular volume expansion.10, 11 In such states of altered intravascular volume and serum sodium concentration there is disagreement as to the factors (volume or sodium) controlling renin release and how they become sensory signals to the juxtaglomerular apparatus.

To investigate the relative importance of intravascular volume and serum sodium concentration on PRA we have studied diuretic-treated hypertensive patients before and after rapid expansion with solutions that caused similar changes in intravascular volume, but dissimilar changes in serum sodium concentration. We selected diuretic-treated patients because they have been found to have elevated PRA in association with diminished intravascular volume.6, 7


Intravascular volume was rapidly expanded in the 21 patients by administering either 6% dextran in 5% glucose (6DG), or 6% dextran in normal saline solution (6DS). The age, sex, diagnosis, and therapy is presented in Table 1. All hypertensive patients had had complete investigative studies, including renal arteriography. Nineteen were considered to have essential hypertension; in one, hypertension was thought to be secondary to renal artery disease, and in another, to chronic



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