Characterization of postjunctional alpha-1 and alpha-2 adrenoceptors activated by exogenous or nerve-released norepinephrine in the canine saphenous vein Academic Article uri icon

Overview

MeSH Major

  • Norepinephrine
  • Receptors, Adrenergic, alpha
  • Saphenous Vein
  • Sympathetic Nervous System

abstract

  • Experiments were designed to characterize alpha-1 and alpha-2 adrenoceptor-mediated effects in the canine saphenous vein. Rings of saphenous vein were mounted for isometric tension recording in physiological saline solution. Contractile responses evoked by alpha-1 adrenoceptor agonists, cirazoline or St 587 were inhibited by alpha-1 antagonists, prazosin (pA2 = 7.9) or phenoxybenzamine, but were relatively resistant to the alpha-2 adrenoceptor antagonist rauwolscine. The responses to alpha-2 adrenoceptor agonists, xylazine or B-HT 920, were relatively resistant to prazosin or phenoxybenzamine but were antagonized by rauwolscine (pA2 = 8.7). After phenoxybenzamine, the alpha-2 agonists, M-7, guanfacine, UK 14304, B-HT 920 and xylazine evoked similar maximal increases in tension which were considerably smaller (approximately 50%) than that attained by alpha-1 adrenoceptor stimulation. The different concentration-effect characteristics of these responses were also revealed using norepinephrine. Prazosin produced a biphasic effect on the concentration-response curve of norepinephrine, being more potent against responses above 50% of the maximum (pA2 = 7.9) compared to lower increases in tension (pA2 = 6.2). After alpha-1 adrenoceptor blockade with prazosin, rauwolscine was more effective against responses below 50% of the maximum, compared to higher increases in tension. The results suggest that the alpha-1 and alpha-2 adrenoceptor-mediated concentration-effect curves to norepinephrine are almost coincident and that alpha-2 adrenergic stimulation produces only partial activation of the vascular smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

publication date

  • January 1984

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 6088763

Additional Document Info

start page

  • 699

end page

  • 705

volume

  • 230

number

  • 3