Contribution of adenosine to changes in coronary flow in metabolically stimulated rat heart.
The extent to which endogenous, extracellular adenosine mediates increased coronary flow in crystalloid-perfused, isovolumic rat hearts stimulated with either norepinephrine or isoproterenol was examined. When infused into the coronary circulation, norepinephrine (1 x 10(-7) M) rapidly increased left ventricular developed pressure (LVDP) from 81 +/- 6 to 235 +/- 13 mmHg (1 mmHg = 133.3 Pa) and coronary flow from 12.7 +/- 0.8 to 18.4 +/- 0.7 mL.min-1.g-1. The presence of either adenosine deaminase (2 U.mL-1) or the adenosine receptor antagonist, 8-phenyltheophylline (5 x 10(-6) M) in the perfusate of norepinephrine-stimulated hearts augmented the increase in LVDP and +/- dP/dtmax by 10-20% but reduced the increase in coronary flow by 34%. Doubling the rate of adenosine deaminase infusion, or infusing the enzyme and 8-phenyltheophylline together did not alter their inhibitory effectiveness. Similar results were observed with hearts stimulated with isoproterenol (5 x 10(-8) M). These data show that about a third of the vasodilation that results from the metabolic stimulation of rat heart by catecholamines is due to the receptor-mediated action of extracellular adenosine.
Headrick
J
J
School of Science, Griffith University, Nathan, Australia.
Willis
R J
RJ
D000241:Adenosine / Q000502:physiology*; D000243:Adenosine Deaminase / Q000032:analysis / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008970:Molecular Weight; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D011983:Receptors, Purinergic / Q000378:metabolism
D011983:Receptors, Purinergic; D000243:Adenosine Deaminase; D000241:Adenosine; D007545:Isoproterenol; D009638:Norepinephrine