Influence of renal sympathectomy, sodium depletion and prostaglandin synthetase inhibition on prostaglandin production and [3H]PGE2binding characteristics in rat kidney

Publisher Website
Google Scholar
Abstract
The effects of renal sympathectomy (unilateral, renal microsurgical denervation), sodium depletion (hypovolemia) and prostaglandin synthetase inhibition on the rate of prostaglandin synthesis and [3H]PGE2binding characteristics were studied in the rat kidney. The intrarenal rate of prostaglandin synthesis was measured by monitoring the urinary excretion of 6‐keto‐PGFlα, the stable hydration product of prostacyclin. Dietary sodium restriction was associated with a 99% decrease in urinary sodium excretion (P< 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‐PGF1αnor the density or affinity of [3H]PGE2binding sites as compared to control. However, in sodium‐depleted rats, prostaglandin synthesis inhibition, induced by naproxen, decreased the urinary excretion of 6‐keto‐PGF1αby 40% (P= 0.011) and increased the number of [3H]PGE2binding 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‐PGFla, and did not modulate the [3H]PGE2binding characteristics. The lack of effect on the excretion of 6‐keto‐PGF1aand on the [3H]PGE2binding characteristics supports the view that sulindac spares renal prostaglandin synthesis.