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Department of Surgery and Vascular Biology Research Group, University of Kentucky College of Medicine, Lexington, Kentucky 40536
The purpose of this study was to compare the
hemodynamic effects of the adenosine
A3-receptor agonists
N6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-
-D-ribofuranosyl]adenine (IB-MECA) and
2-chloro-N6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)--D-ribofuranosyl]adenine (Cl-IB-MECA) in isolated rat and rabbit hearts and in the intact, open-chest pig. Isolated hearts perfused with Krebs-Henseleit buffer at
a constant pressure (70 mmHg) were treated with 50 nM of either IB-MECA
or Cl-IB-MECA. Neither IB-MECA nor Cl-IB-MECA altered ventricular
function or heart rate in the isolated rat and rabbit hearts, and
neither agent altered coronary flow in the rabbit. However, 2 min of
IB-MECA treatment in the isolated rat heart increased coronary flow by
25%, an effect that did not exhibit tachyphylaxis. The IB-MECA-induced
coronary dilation was only partially attenuated by the adenosine
A3-receptor antagonist MRS-1191
(50 nM). IB-MECA-induced coronary dilation was completely blocked by
the adenosine A2a-receptor
antagonist
7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (Sch-58261, 50 nM). Cl-IB-MECA (50 nM) did not increase coronary flow
in the rat, but 100 nM did increase flow by 18%. In pentobarbital sodium-anesthetized pigs IB-MECA (5 µg/kg iv) decreased systemic blood pressure and increased pulmonary artery pressure, effects that
did exhibit tachyphylaxis. These results illustrate that adenosine
A3-receptor agonists produce
species-dependent effects, which in the rat heart appear to be caused
by adenosine A2a-receptor activation.
isolated heart; rat; rabbit; in vivo pig; coronary flow; blood pressure
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