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.
D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D005919:Glomerular Filtration Rate; D007213:Indomethacin / Q000494:pharmacology; D011141:Polyuria / Q000209:etiology*; D011458:Prostaglandins E / Q000378:metabolism; D012078:Renal Artery Obstruction / Q000150:complications*; D012083:Renin / Q000097:blood; D012504:Saralasin / Q000494:pharmacology; D012964:Sodium / Q000652:urine; D014294:Trimethaphan / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
D011458:Prostaglandins E; D014667:Vasopressins; D014294:Trimethaphan; D012964:Sodium; D012083:Renin; D012504:Saralasin; D007213:Indomethacin