Adenosine-induced Coronary Vasodilation Research Articles

The effect of alpha adrenergic block on adenosine- and ATP-induced coronary vasodilation.

A current theory of regulation of coronary blood flow is that of adenosine-induced coronary vasodilation (1). In particular, the hypothesis that a local increase in the extracellular concentration of adenosine is responsible for the reactive hyperemia of temporary coronary occlusion has gained support from the recent work of several investigators (2, 3). Although there is evidence that adenosine is formed through the degradation of the adenine nucleotides in response to myocardial hypoxia (3), the mechanisms by which coronary vasodilation is produced is unknown. A recently reported study in isolated guinea pig and rat hearts suggested that adenosine causes coronary vasodilation by inhibition of alpha adrenergic activity in the coronary resistance vessels and that the effect can be competitively blocked by alpha adrenergic blockade (4). Since myocardial reactive hyperemia has been shown to be unaffected by alpha adrenergic blockade (5), confirmation of inhibition of adenosine induced coronary vasodilation ...

DIFFERENCES AMONG DIPYRIDAMOLE, CARBOCHROMEN AND LIDOFLAZINE IN RESPONSES OF THE CORONARY AND THE RENAL ARTERIES

Chemical compounds which are used as coronary vasodilators in the clinic may be divided into specific and non-specific groups. Dipyridamole (1), carbochromen (2) and lidoflazine (3) belong to the former, while nitroglycerin and papaverine derivatives are typical drugs belonging to the latter. Since Bretschneider (4) discovered in 1962 that dipyridamole potentiated hypotensive response to adenosine, extensive studies have been published as to the effect of dipyridamole on adenosine metabolism. Miura et al. (5) observed a marked potentiation of adenosineinduced coronary vasodilation after dipyridamole treatment. On the other hand, Hashimoto et al. (6) described that dipyridamole induced a vasoconstriction in the renal artery similar to the effects of AMP or adenosine. Sakai et al. (7) found that in the renal artery dipyridamole potentiated vasoconstrictor response not only to adenosine and AMP but also to norepinephrine. Recently, the authors (8) confirmed a potentiation of coronary vasodilator response to norepinephrine after dipyridamole treatment. In this paper, the effects of dipyridamole, carbochromen and lidoflazine on the renal and the coronary vessels have been compared. A constant volume perfusion was arranged and the change in perfusion pressure was recorded. Drug solution, 0.1 ml was injected intra-arterially in a period of 10 sec.. The continuous administration of drug solution was performed using a Harvard infusion pump (Model 600/900). Dipyridamole was infused at a rate of 0.01 and 0.1 μg/min and carbochromen or lidoflazine was infused at the rate of 0.1 and 1.0 μg/min.