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Stimulation of Renal Prostaglandins by Pressor Hormones in Man: Comparison of Prostaglandin E2 and Prostacyclin (6 Keto prostaglandin F₁)^*

Los Angeles County/University of Southern California Medical Center, Department of Medicine, Section of Endocrinology, Los Angeles, California 90033

Address requests for reprints to: Dr. Jerry Nadler, Department of Medicine, Los Angeles County Medical Center, Los Angeles, California 90033.

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 F₁ 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 < 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 F₁ (from 34.6 ± 8 to 56.1 ± 9 ng/4 h, P < 0.02). -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 Metab 56:1260,1983)

^* This work was supported by Grants HL-21112, AM26487 and RR-43 from the NIH and was presented in part at the International Prostaglandin Conference, Florence, Italy, 1982.

Received June 26, 1982.