In previous studies, we have demonstrated that intravenous (i.V.) infusion of BW373U86 (BW), a non-peptide opioid agonist, produced a significant increase in urine flow rate (V) and urinary sodium excretion (UMV). To characterize the subtype(s) of the opioid receptor(s) that mediates the renal effects of BW, we examined the renal responses produced by BW infusion in conscious Sprague-Dawley rats (n=5), or in rats pretreated with naltrindole (n=7), a selective delta opioid receptor antagonist. Rats were chronically instrumented with femoral arterial and venous catheters and a bladder cannula for collection of urine samples. During continuous isotonic saline infusion (55 μl/min, i.v.), changes in V and UNaV were measured during control (20 min) and during six consecutive experimental periods (10 min ea) after the start of BW infusion (50 μg/kg/min, i.v.). Renal responses to BW infusion were also examined in rats pre-treated with naltrindole (1 mg/kg, i.v.). Results: BW produced a significant increase in V (22.5±3.5 to 54.2±4.8 μl/min/gKw) and UNaV (4.0±0.6 to 5.9±0.6 μeq/min/gKw) 30 min after the start of infusion. In contrast, in rats pretreated with naltrindole, BW did not alter V or UNaV throughout the protocol. In other studies, naltrindole pretreatment did not alter the renal responses produced by the kappa or mu-opioid agonists, U-50488H (20 μg/kg/min, i.v.) or dermorphin (0.3 mg/kg, i.V.), resp. These results demonstrate that the diuretic and natriuretic responses produced by BW are mediated via a pathway involving delta opioid receptors since the renal responses produced by this opioid are abolished by naltrindole.
|Original language||English (US)|
|State||Published - 1997|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology