Prejunctional alpha 2-adrenoceptors modulate stimulation-evoked norepinephrine release in rabbit lateral saphenous vein.
Segments of rabbit lateral saphenous vein prelabelled with [3H]noradrenaline were perfused and superfused with physiological salt solution. Tritium overflow evoked by transmural nerve stimulation (3 Hz for 2 min) was abolished by tetrodotoxin (1 microM). The selective alpha 2-adrenoceptor agonist UK 14,304 inhibited stimulation-evoked 3H-overflow in a concentration-dependent manner, with an IC50 of 71 nM. In contrast, the alpha 2-adrenoceptor agonist B-HT 933 had no effect on 3H-overflow in concentrations up to 10 microM. The selective alpha 2-adrenoceptor antagonists idazoxan and SKF 86466, as well as the non-selective alpha-antagonist phentolamine, facilitated the nerve stimulation evoked 3H-overflow, with an order of potency of idazoxan greater than or equal to phentolamine greater than SK&F 86466. Prazosin (100 nM) had little effect on 3H-overflow. These findings suggest that stimulation-evoked neurotransmitter release is modulated via prejunctional alpha 2-adrenoceptors.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D011817:Rabbits; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012501:Saphenous Vein / Q000378:metabolism
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D009638:Norepinephrine