The effect of prostaglandin-synthesis stimulation and blockade on sodium excretion at a fixed renal perfusion pressure.

PGE synthesis was increased by an infusion of AA and decreased with indomethacin or carpofen. Intrarenal infusions of arachidonate increased RBF from 222 +/- 37 to 275 +/- 51 ml/min (p less than 0.05) and UNaV from 85 +/- 23 to 121 +/- 32 muEq/min (p less than 0.05), with renal vein PGE increasing from 0.41 +/- 0.08 to 1.81 +/- 0.69 ng/ml (p less than 0.05). However, when renal perfusion pressure was reduced and maintained constant at 82 +/- 4 mm Hg during the AA infusion, RBF, and UNaV did not change, 185 +/- 26 vs. 178 +/- 21 ml/min and 10 +/- 3 vs 8 +/- 3 muEq/min, respectively, although renal vein PGE increased from 0.8 +/- 0.2 to 1.95 +/- 0.52 ng/ml (p less than 0.05. During Pl with indomethacin, 2 mg/kg, RBF fell from 210 +/- 27 to 120 +/- 16 ml/min (p less than 0.05), and UNaV diminished from 39 +/- 6 to 22 +/- 10 muEq/min (p less than 0.05), as renal vein PGE decreased from 0.37 +/- 0.04 to 0.19 +/- 0.03 ng/ml (p less than 0.05). When renal perfusion pressure was reduced and maintained constant at 90 +/- 2 mm Hg, renal vein PGE fell from 0.72 +/- 0.29 to 0.20 +/- 0.08 ng/ml (p less than 0.05), whereas RBF and UNaV were unchanged during Pl, 172 +/- 20 vs. 166 +/- 30 and 33 +/- 15 vs. 28 +/- 11, respectively. The results indicate that the change in sodium excretion with variation in prostaglandin synthesis is best explained by concomitant changes in RBF.

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.