β-Adrenoceptor density and responsiveness were examined in rat vas deferens following surgical and pharmacological treatments. Receptor density was measured by Scatchard analysis of saturation isotherms of specific [125I]pindolol ([125I]PIN) binding in membrane homogenates. Functional responsiveness was measured by isoprenaline-induced inhibition of field stimulated (60 V, 1 ms, 0.1 Hz) or 40 mM K+-induced contractions. Four days following surgical denervation of vas deferens there was no change in the density of [125I]PIN binding sites, suggesting that these sites are not located on prejunctional neurons. Neither 7 day bilateral adrenalectomy, 21 day denervation, nor 7 days treatment with 10 mg/kg per day desmethylimipramine caused changes in either the potency of isoprenaline in inhibiting contraction or the density of [125I]PIN binding sites compared to controls. Infusion of 3 mg/kg per day isoprenaline for 8 days significantly reduced the potency of isoprenaline in inhibiting field stimulated contractions, reduced the maximum degree of inhibition, and reduced the density of [125I]PIN binding sites. These results suggest that β-adrenoceptor density and responsiveness in rat vas deferens are not affected by removal of adrenal hormones or neuronal stimulation, but that receptor density and responsiveness can be decreased by increasing the concentration of β-adrenoceptor agonists at the receptor. Therefore, β-adrenoceptors in rat vas deferens probably receive little tonic stimulation under normal circumstances.
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