Hayes A G, Skingle M, Tyers M B
J Pharmacol Exp Ther. 1987 Mar;240(3):984-8.
The effects of a series of opioid drugs on urine output in the water-loaded rat were studied and also the block of those effects by the irreversible opioid receptor antagonist, beta-funaltrexamine (beta-FNA). Fentanyl, d-propoxyphene, profadol, bromadoline, buprenorphine and nalbuphine produced only a decrease in urine output, which was antagonised by pretreatment with beta-FNA, 40 mg/kg s.c., 24 hr beforehand. These drugs were thus characterized as selective mu receptor agonists. U-50,488, tifluadom, Mr2034, proxorphan, ethylketocyclazocine and butorphanol all produced an initial decrease in urine output, which was antagonized by beta-FNA, and therefore probably mu receptor mediated, followed by a beta-FNA insensitive diuretic effect, which was probably kappa receptor mediated. For U-50,488, tifluadom, Mr2034 and proxorphan the threshold dose for increasing urine output was lower than that for decreasing it, suggesting that these four compounds are kappa-selective agonists. For ethylketocyclazocine and butorphanol, the threshold doses for producing both effects were similar, suggesting that these two drugs are non-selective agonists. SKF 10,047 produced a diuretic effect at low dose-levels, which may be kappa receptor mediated, and a beta-FNA insensitive decrease in urine output at higher dose-levels, which may suggest a sigma receptor mediated effect.
