Sustained increase in rat myocardial alpha 1A-adrenoceptors induced by 6-hydroxydopamine treatment involves a decelerated receptor turnover.

摘要: The biochemical mechanisms involved in the α1-adrenoceptor up-regulation and possible changes subtypes of adrenoceptors rat heart after chemical denervation were investigated. effects acute 6-hydroxydopamine treatment (two increasing doses 24 h apart) on pseudo-steady state densities turnover rates α1-adrenoceptors studied ventricular myocardium rat. We have assessed repopulation kinetics [3H]prazosin binding sites irreversible inactivation induced by a single dose phenoxybenzamine (1 mg/kg i.p.) rats acutely treated either with or vehicle (control animals). Seven days last administration an enhanced density (Bmax 58.7 ± 3.6 fmol/mg protein vehicle-treated versus 82.6 5.3 6-hydroxydopamine-treated rats) was observed. This not accompanied dissociation constant value. Furthermore, proportion high affinity for WB-4101 altered (21 2% 72 3% animals 6-hydroxydopamine, respectively). In myocardium, turnover, evaluated during 6-hydroxydopamine-induced upregulation (7–19 completion 6-hydroxydopamine) revealed increase half-life (t1/2 67.2 38.7 control present study confirms reveals that effect is almost completely confined to α1A-adrenoceptor subtype. α1A-adrenoceptors result decrease cellular processes rate receptor degradation.