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-PGF1 alpha, thromboxane B2 and PGF2 alpha) 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-PGF1 alpha and TXB2 did not vary, and PGF2 alpha 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 PGF2 alpha, but not that of PGE2 and 6-keto-PGF1 alpha. In KCl- rats, TXB2 but not PGF2 alpha 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 alpha and TXB2 increased in both KCl+ and KCl- rats, whereas PGF2 alpha 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.(ABSTRACT TRUNCATED AT 250 WORDS)