Changes in Renal Prostanoid Synthesis Induced by Potassium Loading in Rats

Abstract

Previous works have demonstrated changes in the urinary excretion of prostaglandins (PG) in response to changes in potassium (K) or sodium (Na) intake. In the present study, the production of PGE₂, PGF_2α, 6-keto-PGF_1αand thromboxane B₂ (TXB₂) by isolated glomeruli, cortical homogenates, medullary and papillary slices was measured in K-loaded rats on either a normal or a low Na intake. In glomeruli, K loading increased selectively PGE₂synthesis. In Na-depleted animals, all prostanoids were elevated and K loading did not induce a further increase. In cortical and medullary preparations, PGE₂ was decreased by K loading irrespective of the state of Na balance. In papilla, PGE₂ decreased (in all K-loaded rats) and PGF_2α increased (only in rats with normal Na intake). 6-Keto-PGF_1α and TXB₂ did not change significantly. No correlation was present between changes of PG synthesis and urinary kallikrein excretion. The results demonstrate a specific effect of K on PGE₂ and PGF_2α, and suggest a role for these substances in K homeostasis.