The effect of vasoconstrictive agonists and their nonpressor analogs on renal prostaglandin production was investigated in normal subjects maintained on constant diets. Arginine vasopressin (AVP), 10 U, desamino-d arginine vasopressin (dDAVP), 4 μg, angiotensin II (All), 5 ng/kg-min, des-Asp angiotensin II (AIII), 5 ng/kg-min, norepinephrine (NE), 0.1 μg/kgmin, and NE plus phenoxybenzamine (PHB), 0.8 mg/kg, were administered on separate days. Prostaglandin E₂ (PGE₂) and the stable prostacyclin metabolite, 6 keto prostaglandin F_1α were measured in 4-h urine collections by procedures with high resolution chromatography and RIA using highly specific antisera. AVP and dDAVP similarly reduced urine volume and increased urine osmolality. AII, AIII, NE, and NE + PHB did not alter basal urine volume, osmolality, creatinine, or electrolyte excretion. Blood pressure was similarly increased by All and NE infusions (23 ± 3 vs. 19 ± 2 (SE) mm Hg). AVP and All increased only PGE2 excretion (61 ± 8 to 151 ± 34 ng/4 h for AVP, and 38.7 ± 7 to 75 ± 19 ng/4 h for AII, P <α 0.05). The nonpressor analogs, dDAVP and AIII, had no effect on urinary prostaglandin excretion. In contrast, NE increased both PGE₂ (from 38.7 ± 7 to 74.5 ± 12 ng/4 h, P < 0.02) and 6 keto prostaglandin F_1α (from 34.6 ± 8 to 56.1 ± 9 ng/4 h, P < 0.02). α-Blockade with PHB totally abolished the NE-induced systemic pressor and prostaglandin stimulatory effect.

These data suggest that renal PGE₂ and prostacyclin are not altered in parallel by vasoactive stimuli. PGE₂ appears to be released in response to agents that induce renal vasoconstriction and reduced renal blood flow whereas renal prostacyclin excretion is stimulated by an adrenergic agonist via a-receptor activation and not vasoconstriction per se. (J Clin Endocrinol Metab56:1260,1983)