β 2-Adrenoceptor-mediated inhibition of field stimulation induced contractile responses of the smooth muscle of the rat prostate gland

Abstract

Isolated preparations of rat prostate responded to electrical field stimulation (2 strains every 60 s, 0.5 ms, 10 Hz, 80 V) with contractions. The adrenoceptor agonists adrenaline, isoprenaline and noradrenaline (0.1 nM–10 μM) elicited concentration-dependent inhibition of electrical field stimulation-induced contractions of the rat prostate. Phenylephrine had no effect on the amplitude of electrical field stimulation-induced contractions. The rank order of potency was isoprenaline≥adrenaline=noradrenaline>phenylephrine. Inhibition of electrical field stimulation-induced contractions by isoprenaline was attenuated by propranolol (1 μM). The selective β 1-adrenoceptor agonist (−)-1-(3,4-dimethoxy-phenethylamino)-3-(3,4-dihydroxyphenoxy)-2-propanol)oxalate (RO363) and the selective β 2-adrenoceptor agonist salbutamol (1 nM–100 μM) were approximately equipotent in inhibiting electrical field stimulation-induced contractions but the selective β 3-adrenoceptor agonist sodium 4-(2-[2-hydroxy-{3-chlorophenyl}ethylamino]propyl)phenoxyacetate (BRL 37344, 1 nM–100 μM) did not inhibit electrical field stimulation-induced contractions. The selective β 2-adrenoceptor antagonist, (±)-1-[2,3-(dihydro-7-methyl-1 H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118 551, 0.1 μM) attenuated inhibitory responses to isoprenaline and salbutamol, while the selective β 1-adrenoceptor antagonist atenolol (3 μM) did not. Contractions induced by electrical field stimulation were also inhibited by forskolin (10 nM–3 mM) but unaffected by sodium nitroprusside (10 nM–1 mM) indicating the presence of an inhibitory cAMP mechanism. These data suggest that stimulation of β 2-adrenoceptors can inhibit contractions of the rat prostate induced by electrical field stimulation.