Relaxation by adenosine and its analogs of potassium-contracted human coronary arteries

Naunyn Schmiedebergs Arch Pharmacol. 1990 Apr;341(4):388-90. doi: 10.1007/BF00180667.

Abstract

The present study was an attempt to characterize the adenosine receptor in human coronary arteries, and to establish the dependence of the relaxations mediated by this receptor on a functional endothelium. Human coronary arteries were obtained from organ donors. Adenosine and its analogs (5'-N-ethyl-carboxamido-adenosine, NECA; N6-L-phenylisopropyladenosine, L-PIA; 2-chloroadenosine, CAD), all inhibited the contraction induced by 25 mmol/l KCl in a concentration-dependent manner and the order of potency was found to be: NECA greater than CAD greater than L-PIA greater than adenosine. These relaxations were antagonized by 8-phenyltheophylline (8PT). At higher concentrations of KCl, the relaxations were attenuated. In rings which relaxed in response to endothelium-dependent relaxing agents (bradykinin and A23187), NECA and CAD produced relaxations similar to those produced in rings which did not show endothelium-dependent responses. The results suggest that the coronary adenosine receptor (probably A2) mediates relaxations which may not be dependent on the relaxing function of the endothelium.

MeSH terms

  • 2-Chloroadenosine / pharmacology
  • Adenosine / analogs & derivatives
  • Adenosine / pharmacology*
  • Adenosine-5'-(N-ethylcarboxamide)
  • Adult
  • Coronary Vessels / drug effects
  • Humans
  • In Vitro Techniques
  • Male
  • Muscle Relaxation / drug effects
  • Muscle, Smooth, Vascular / drug effects*
  • Phenylisopropyladenosine / pharmacology
  • Potassium / pharmacology*
  • Receptors, Purinergic / drug effects

Substances

  • Receptors, Purinergic
  • 2-Chloroadenosine
  • Phenylisopropyladenosine
  • Adenosine-5'-(N-ethylcarboxamide)
  • Adenosine
  • Potassium