Article date: June 1982
By: JAMES R. DOCHERTY, KLAUS STARKE in Volume 76, Issue 2, pages 327-335
The α‐adrenoceptor agonists, Clonidine and xylazine, reduced and the α‐antagonists, yohimbine and rauwolscine, increased the stimulation‐evoked tritium overflow from rabbit aorta and portal vein pre‐incubated with [3H]‐noradrenaline.
Based on an order of agonist potency of Clonidine > xylazine > phenylephrine and antagonist potency of rauwolscine = yohimbine > prazosin, the presynaptic receptor mediating these effects is of the α2‐type.
In the aorta, stimulation‐evoked contractions were abolished by prazosin (0.1 μm) and potentiated by rauwolscine and yohimbine in concentrations that increased the stimulation‐evoked overflow of tritium.
In the portal vein, prazosin was less potent in reducing, and rauwolscine and yohimbine failed to potentiate, the stimulation‐evoked contraction.
In experiments in which tissues were pre‐exposed to phenoxybenzamine (30 nM) to block some of the postsynaptic α‐receptors, rauwolscine in concentrations that increased stimulation‐evoked tritium overflow, reduced the evoked contraction in the portal vein but not in the aorta.
It is concluded that presynaptic α2‐autoreceptors are present in both tissues and that the postsynaptic α‐receptors which mediate nerve stimulation‐evoked contractions are α1 in the aorta but a mixture of α1 and α2 in the portal vein.
The α‐adrenoceptor agonists, Clonidine and xylazine, reduced and the α‐antagonists, yohimbine and rauwolscine, increased the stimulation‐evoked tritium overflow from rabbit aorta and portal vein pre‐incubated with [3H]‐noradrenaline.
Based on an order of agonist potency of Clonidine > xylazine > phenylephrine and antagonist potency of rauwolscine = yohimbine > prazosin, the presynaptic receptor mediating these effects is of the α2‐type.
In the aorta, stimulation‐evoked contractions were abolished by prazosin (0.1 μm) and potentiated by rauwolscine and yohimbine in concentrations that increased the stimulation‐evoked overflow of tritium.
In the portal vein, prazosin was less potent in reducing, and rauwolscine and yohimbine failed to potentiate, the stimulation‐evoked contraction.
In experiments in which tissues were pre‐exposed to phenoxybenzamine (30 nM) to block some of the postsynaptic α‐receptors, rauwolscine in concentrations that increased stimulation‐evoked tritium overflow, reduced the evoked contraction in the portal vein but not in the aorta.
It is concluded that presynaptic α2‐autoreceptors are present in both tissues and that the postsynaptic α‐receptors which mediate nerve stimulation‐evoked contractions are α1 in the aorta but a mixture of α1 and α2 in the portal vein.
DOI: 10.1111/j.1476-5381.1982.tb09224.x
View this article