Influence of renal sympathectomy, sodium depletion and prostaglandin synthetase inhibition on prostaglandin production and [3H]PGE2 binding characteristics in rat kidney

Acta Physiologica Scandinavica
L O ErikssonK E Andersson

Abstract

The effects of renal sympathectomy (unilateral, renal microsurgical denervation), sodium depletion (hypovolaemia) and prostaglandin synthetase inhibition on the rate of prostaglandin synthesis and [3H]PGE2 binding characteristics were studied in the rat kidney. The intrarenal rate of prostaglandin synthesis was measured by monitoring the urinary excretion of 6-keto-PGF1 alpha, the stable hydration product of prostacyclin. Dietary sodium restriction was associated with a 99% decrease in urinary sodium excretion (P less than 0.001) and a 17% decrease of urine volume (n.s.). Renal denervation or sodium deprivation changed neither the rate of excretion of 6-keto-PGF1 alpha nor the density or affinity of [3H]PGE2 binding sites as compared to control. However, in sodium-depleted rats, prostaglandin synthesis inhibition, induced by naproxen, decreased the urinary excretion of 6-keto-PGF1 alpha by 40% (P = 0.011) and increased the number of [3H]PGE2 binding sites by almost 30% (P = 0.031) with no change in binding affinities as compared with sodium-depleted controls. In contrast, sulindac was not able to suppress the renal synthesis and excretion of 6-keto-PGF1 alpha, and did not modulate the [3H]PGE2 binding characteristics. The lack ...Continue Reading

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