An attempt to characterize alpha-adrenoceptors on human dorsal foot veins in situ.
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.
Barthel
W
W
Institut für Klinische Pharmakologie der Medizinischen Hochschule Erfurt, Germany.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000328:Adult; D003000:Clonidine / Q000494:pharmacology; D005528:Foot / Q000098:blood supply*; D006801:Humans; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects; D014680:Veins / Q000187:drug effects / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D010656:Phenylephrine; D003000:Clonidine