Reverse trans-synaptic regulation of catecholamine synthesis in adrenergic neurones

摘要: Abstract It was established that the blocking agent of beta-adrenoceptors, propanolol (1 × 10−6M), activates [3H]catecholamine synthesis from [3H]tyrosine in isolated rat organs (vas deferens and atrium) by 40–80%. The alpha-adrenoceptors, phentolamine 10−6M) [3H]catecholanune 30–60% only organ possessing postsynaptic alpha-adrenoceptors deferens). activator isopropylnoradrenaline shown to produce a decrease 30–40% both investigated. substance activating phenylephrine 10−5M), inhibits with 40–50%. Activation inhibition induced adrenotropic drugs is due release chemical factors effector cell their influence on adrenergic neurone. formation changing intensity catecholamine related activation protein cell. processes which proceed neurone are not connected de novo. Existence common mechanism for reverse trans-synaptic regulation noradrenergic uptake via adrenoceptors discussed.