Vascular alpha 2-adrenoceptors can mediate nerve stimulation-evoked contractions.
It is now established that alpha 2-adrenoceptors can be present on vascular smooth muscle as targets for exogenous agonists, but some controversy exists as to whether these vascular alpha 2-receptors may also be the target for neurally released noradrenaline. In human saphenous vein we have found evidence that the alpha 2-antagonist yohimbine in low concentrations (0.01 mumol/l) can significantly inhibit stimulation-evoked contractions, whereas the alpha 1-antagonist prazosin is more than ten times less potent. It is concluded that, at least in some tissues, neuro-effector transmission can be mediated by vascular alpha 2-adrenoceptors.
Docherty
J R
JR
Hyland
L
L
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D000818:Animals; D004558:Electric Stimulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009469:Neuromuscular Junction / Q000187:drug effects; D011224:Prazosin / Q000494:pharmacology; D011817:Rabbits; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012501:Saphenous Vein; D009435:Synaptic Transmission / Q000187:drug effects*; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D011224:Prazosin