Release of prostaglandin I2 from hog kidney by propranolol.
Prostaglandin I2 (PGI2) decreases blood pressure. Perfusion of isolated hog kidney by propranolol in modified Krebs-Ringer solution resulted in a significant increase in 6-keto-prostaglandin F1 alpha, the major metabolite of PGI2. Prostaglandin E2 and renin activity remained unchanged. Because the concentration of PGI2-like substance in the renal vein has been shown to be greater than in the renal artery after bradykinin infusion, a contribution of PGI2 to the regulation of blood pressure was proposed. Isoproterenol has been shown to augment urinary kallikrein, but the effect of urinary kallikrein on propranolol is unclear. With a modified Krebs-Ringer solution free of plasma kininogen, a renin substrate, it was concluded that propranolol (1) induces PGI2 release from the kidney, which may contribute to a direct antihypertensive action of this beta-adrenergic blocking agent, and (2) decreases urinary kallikrein.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003404:Creatinine / Q000652:urine; D015232:Dinoprostone; D011464:Epoprostenol / Q000378:metabolism*; D066298:In Vitro Techniques; D007610:Kallikreins / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology*; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D013552:Swine; D010130:p-Aminohippuric Acid / Q000378:metabolism
D011453:Prostaglandins; D011458:Prostaglandins E; D011433:Propranolol; D003404:Creatinine; D011464:Epoprostenol; D007610:Kallikreins; D015232:Dinoprostone; D010130:p-Aminohippuric Acid