Postobstructive diuresis. Studies in a dialyzed patient with a solitary kidney.
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The effect of dynorphin A-(1-13) on morphine-induced urine output was studied in the rat. The previous simultaneous intracerebroventricular (i.c.v.) injection of dynorphin (20 micrograms/rat) and morphine (20 micrograms/rat) altered the response of rat given morphine (20 micrograms/rat) 24 h later, producing a 3-fold increase in urine output. In contrast, previous injection of dynorphin or morphine alone had no effect.
(+)-Tifluadom injected i.p. produced a biphasic response of urine output: within the first hour of its administration the drug produced antidiuresis followed by a diuretic phase. In contrast, the (-) isomer produced a modest reduction in urine output as compared to the output of the saline-treated rats. In addition, (+)-tifluadom markedly reduced the output of urinary Na+ and K+. The effects of (+)-tifluadom were blocked by 7.5 mg/kg naloxone but not by 10 mg/kg of the benzodiazepine antagonist Ro 15-1788. Parallel experiments demonstrated that the i.v. administration of (+)-tifluadom to non-anesthetized rats caused a dose-related pressor response that lasted for at least 15 min. This effect of (+)-tifluadom was blocked and antagonized by naloxone. In contrast, (-)-tifluadom was either inactive on the cardiovascular system or produced short-lasting hypotension. In pentobarbital-anesthetized rats, 100 micrograms/kg (+)-tifluadom caused a precipitous hypotension that was reversed by naloxone but not by Ro 15-1788.
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