Interactions between the renin-angiotensin system and prostanoids in modulating renal function in potassium-depleted healthy women

Abstract

Plasma renin activity (PRA) and urinary aldosterone excretion were determined in healthy women with normal potassium balance (N, n = 20) or experimental potassium depletion (KD). KD was induced by natriuretic treatment — associated with replacement of net NaCl and water losses — and low dietary potassium intake (≤ 10 mmol/d). By using different depletion patterns, three groups were obtained with cumulative potassium deficits (mean ± SEM) of 160 ± 43 (KD1, n = 8), 198 ± 22 (KD2, n = 6) and 215 ± 54 mmol (KD3, n = 6). The renal function by the clearance (cl.) method and urinary concentrations of prostaglandin E 2 (PGE 2), 6-keto-PGF 1α (6KPGF), and thromboxane B 2 (TXB 2) by the RIA method were estimated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by low-dose infusion of lysine-8-vasopressin (LVP). 1. 1. In all KD groups the depletion treatment significantly reduced both potassium plasma concentration (P K) and urinary potassium excretion while it increased basal PRA; the basal urinary aldosterone excretion was not significantly different from normokalemic controls. In the KD3 vs KD1 group the P κ value was significantly lower. 2. 2. In both KD2 and KD3 groups as compared to the N group, several hypokalemic-like renal dysfunctions — absent in the KD1 group — occurred. Particularly, in the KD2 + KD3 vs N group the renal ability in both urine diluting (water load) and concentrating (LVP infusion) was significantly impaired. 3. 3. In the KD2 vs N group during polyuria the urinary excretions of the three prostanoids were significantly lower, while in the KD3 vs N group only that of PGE 2 was significantly lower. During LVP infusion in both KD2 and KD3 vs N group the differences in urinary prostanoid excretions were attenuated. The data suggest that a pathophysiologically critical degree of KD depressed the dynamic response of renal prostanoid synthesis to polyuria. However, in connection with and probably because of higher values of PRA, the hyporeactivity to polyuria of the renal synthesis of 6KPGF and TXB 2 precursors was corrected.