Stimulation of renal prostanoid synthesis by potassium loading in the rat

In vitro we measured the urinary excretion and synthesis of prostaglandins (PGE₂, 6-keto-PGF(1α), thromboxane B₂ and PGF(2α)) by isolated glomeruli, cortical homogenates, medulla and papilla in KCl-loaded rats (KCl +, average K intake: 17 mmol/day for 20 days) and in rats loaded with non-Cl K salts (KCl-, average K intake: 21 mmol/day) as compared with control rats. In 2 separate groups of rats (KCl+ and KCl-) the urinary excretion of prostaglandins was measured after variations of K intake from an average of 4 to 20 mmol/day in 5-day periods. Glomerular PGE₂ synthesis tended to decrease in KCl+, whereas it increased in KCl- rats. 6-Keto-PGF(1α) and TXB₂ did not vary, and PGF(2α) decreased in both K-loaded groups. In the cortex, KCl loading decreased PGE₂ synthesis. In KCl-, cortical TXB₂ decreased. In the medulla, KCl loading increased the synthesis of TXB₂ and PGF(2α), but not that of PGE₂ and 6-keto-PGF₁(1α). In KCl- rats, TXB₂ but not PGF(2α) increased and PGE₂ synthesis was also elevated. In the papilla, TXB₂ synthesis increased in both KCl+ and KCl- rats. The urinary excretion of 6-keto-PGF₁(1α) and TXB₂ increased in both KCl+ and KCl- rats, whereas PGF(2α) increased only in KCl+ rats. The changes of glomerular prostaglandin synthesis during K loading could dilate the glomerular vasculature, in keeping with the known vasoactive effects of the cation. The altered balance between PGF₂/prostacyclin and TXA₂/PGF(2α) in response to KCl loading could facilitate K excretion by different mechanisms: (1) medullary vasoconstriction, contributing to conservation of interstitial K concentration; (2) stimulation of cortical-collecting duct hypertrophy, and (3) a direct effect on K channels, dependent on intracellular Ca²⁺ levels. The contrasting effects of loading with non-Cl K salts on prostaglandin synthesis would have effects opposite to those of KCl. Since loading with anions less permeant than Cl promotes kaliuresis by directly influencing the electrochemical gradient for K transport, the observed alterations of nonglomerular prostanoid synthesis in KCl- rats could counteract excessive kaliuresis induced by the nonreabsorbable anions.