MODULATION BY β‐ADRENORECEPTORS OF SPONTANEOUS CONTRACTIONS OF RAT URINARY BLADDER

1 Propranolol (0.1 mg/kg i.v.) but not metoprolol (0.2 mg/kg i.v.) pretreatment increased the spontaneous motility triggered by progressive filling of rat urinary bladder without a concomitant effect on bladder capacity, except at high filling volumes. Compared to controls, the spontaneous motility of urinary bladder in propranolol pretreated rats displayed a higher frequency, indicating the existence of a tonic sympathetic inhibition. 2 beta-adrenoreceptor stimulation by isoprenaline (0.1-10 microgram/kg i.v.) or terbutaline (0.1-1 mg/kg i.v.) in vivo produced a dose dependent inhibition of bladder spontaneous motility which was antagonized by propranolol (0.1 mg/kg i.v.) but not by metoprolol (0.2 mg/kg i.v.). Propranolol (0.2 mg/kg i.v.) pretreatment did not antagonize the inhibition of bladder motility produced by intravenous papaverine (0.5 mg/kg). 3 Propranolol (0.1 mg/kg i.v.) significantly antagonized the isoprenaline-induced tachycardia (beta 1 mediated) and fall in diastolic blood pressure (beta 2 mediated) while metoprolol (0.2 mg/kg i.v.) antagonism was confined to beta 1 mediated responses. 4 Isoprenaline (0.25-1.5 microM) inhibited in a concentration dependent manner field stimulation induced contractions of rat detrusor muscle strips as did tetrodotoxin (0.5 microM). Hexamethonium (50 microM) had no inhibitory effect. 5 Our in vivo findings support the view that beta 2-adrenoreceptors are responsible for modulating bladder motility mainly by suppressing the onset of spontaneous contractions.