Barthel W
Institut für Klinische Pharmakologie der Medizinischen Hochschule Erfurt, Germany.
Int J Clin Pharmacol Ther Toxicol. 1993 Jun;31(6):267-70.
The effects of specific alpha-adrenergic agonists and antagonists on the congestion-induced change in the vessel diameter were studied in human dorsal foot veins in situ by means of a linear variable differential transformer. The specific agonist at alpha-1-adrenoceptors, phenylephrine, induced venoconstriction, whereas clonidine, the specific agonist at alpha-2-adrenoceptors, in this regard was ineffective, but on the contrary, lowered the phenylephrine-induced increase in venous tone. The phenylephrine-induced reaction could be inhibited in the rank order of their effectiveness by prazosin, the specific antagonist at alpha-1-adrenoceptors, by sodium nitroprusside and by verapamil. These results are in favour of the assumption that in exogenous stimulation of human foot veins by adrenergic agonists in situ, alpha-1-adrenoceptors are especially involved.