title: Beta2-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) x microM) 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> or =adrenaline=noradrenaline>phenylephrine. Inhibition of electrical field stimulation-induced contractions by isoprenaline was attenuated by propranolol (1 microM). The selective beta1-adrenoceptor agonist (-)-1-(3,4-dimethoxy-phenethylamino)-3-(3,4-dihydroxyphenoxy)-2-propanol)oxalate (RO363) and the selective beta2-adrenoceptor agonist salbutamol (1 nM(-100) x microM) were approximately equipotent in inhibiting electrical field stimulation-induced contractions but the selective beta3-adrenoceptor agonist sodium 4-(2-[2-hydroxy-[3-chlorophenyl]ethylamino]propyl)phenoxyacetate (BRL 37344, 1 nM(-100) x microM) did not inhibit electrical field stimulation-induced contractions. The selective beta2-adrenoceptor antagonist, (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118 551, 0.1 microM) attenuated inhibitory responses to isoprenaline and salbutamol, while the selective beta1-adrenoceptor antagonist atenolol (3 microM) did not. Contractions induced by electrical field stimulation were also inhibited by forskolin (10 nM(-3) x mM) but unaffected by sodium nitroprusside (10 nM(-1) x mM) indicating the presence of an inhibitory cAMP mechanism. These data suggest that stimulation of beta2-adrenoceptors can inhibit contractions of the rat prostate induced by electrical field stimulation.
authors.affiliation: Department of Pharmacology, Monash University, Clayton, Vic. 3800, Australia.
authors.forename: P J
authors.initials: PJ
authors.lastname: Kalodimos
authors.forename: S
authors.initials: S
authors.lastname: Ventura
mesh_terms: D058666:Adrenergic beta-2 Receptor Agonists; D058672:Adrenergic beta-2 Receptor Antagonists; D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D002396:Catechols / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D004558:Electric Stimulation; D004594:Electrophysiology; D004983:Ethanolamines / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011467:Prostate / Q000294:innervation* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects*
chemical_list: D058666:Adrenergic beta-2 Receptor Agonists; D058672:Adrenergic beta-2 Receptor Antagonists; D002396:Catechols; D004983:Ethanolamines; D011412:Propanolamines; D018343:Receptors, Adrenergic, beta-2; D009599:Nitroprusside; D005576:Colforsin; C026777:ICI 118551; D001262:Atenolol; C057368:BRL 37344; C018420:Ro 363; D011433:Propranolol; D000420:Albuterol; D009638:Norepinephrine