The operation of autoregulatory feedback loops in noradrenergic transmission to cardiovascular effector tissues.
The effects of alpha-adrenoceptor blocking drugs on circulating catecholamines or neurogenically released noradrenaline will depend on their relative selectivity for prejunctional or postjunctional alpha-adrenoceptors. Relatively selective prejunctional alpha-adrenoceptor antagonists will block the inhibitory feedback mechanism at sympathetic nerve terminals, thus increasing transmitter release, which will tend to overcome any postjunctional alpha-adrenoceptor blockade, and responses to sympathetic nerve stimulation will be resistant to blockade. They will have noradrenolytic activity in doses which are not sympatholytic; they may even enhance sympathetic nerve activity. In contrast, selective postjunctional alpha-adrenoceptor blocking drugs will be noradrenolytic and sympatholytic. Prazosin has weak prejunctional alpha-adrenoceptors blocking activity, but is relatively selective for postjunctional alpha-adrenoceptors. Yohimbine is relatively selective for prejunctional alpha-adrenoceptors, and phentolamine is not highly selective. Selectivity for postjunctional alpha-adrenoceptors appears to be a desirable action for an antihypertensive drug of this type.
D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000818:Animals; D002319:Cardiovascular System / Q000294:innervation*; D005246:Feedback; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D009638:Norepinephrine / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology; D009435:Synaptic Transmission
D000317:Adrenergic alpha-Antagonists; D013565:Sympatholytics; D009638:Norepinephrine