(292) THE ROLE OF PRE-SYNAPTIC β1-ADRENOCEPTORS IN RAT ISOLATED EPIDIDYMAL VAS DEFERENS CONTRACTILITY

Abstract Introduction The absence of a low-affinity site for propranolol after reserpinisation or rauwolscine treatment suggests a dependence on intact catecholamine stores and α2-adrenoceptors, reflecting β-blockers’ action. In guinea-pig vas deferens, β-adrenoceptor activation increases noradrenaline release while decrease ATP release. Isoprenaline reduces nerve-induced responses in rat vas deferens. Objective To investigate the effect of presynaptic beta 1 adrenergic agonists in rat vas deferens. Methods Adult male Wistar rats were euthanized with isoflurane, then epididymal vas deferens were isolated, placed in Krebs–Henseleit’s solution, and mounted in tissue baths for isometric tension recording using a PowerLab system. The effect of β-adrenoceptor agonist RO363 (100 nM), and antagonists betaxolol (1 μM), metoprolol (1 μM), and atenolol (1 μM) on adrenaline (ADR), noradrenaline (NA) and dopamine (DA) induced contractile responses was assessed. Electric-field stimulation (EFS) and the effect of the sodium channel antagonist tetrodotoxin (TTX 1 μM) were also evaluated. All the procedures were approved by an Ethic Committee. Data were analyzed using nonlinear regression to determine pEC50 values and expressed as mean ± SEM. Results The data showed that RO363 had no effect on DA but caused a concentration-dependent leftward shift on the NA and ADR curves, abolished by TTX pretreatment. RO363 enhanced tissue contraction in response to EFS across all frequencies. Atenolol, betaxolol and metoprolol abolished the effect of RO363 on NA and ADR curves. Conclusions Findings reveal that the β1-adrenoceptor agonist RO363 selectively modulates contractile responses to NA and ADR, indicating a specific interaction with these neurotransmitters sensitive to sodium channel blockade by TTX. The abolition of RO363’s effect by β1-adrenoceptor antagonists further underscores the specificity of β1-adrenoceptor involvement. Results suggest that β1-adrenoceptors are crucial in regulating neurotransmitter-induced contractility in the vas deferens, potentially through mechanisms dependent on intact catecholamine stores and α2-adrenoceptors. This study enhances understanding of adrenergic modulation in male reproductive physiology and may inform future research on pharmacological manipulation of vas deferens contractility. Disclosure No.