The present study was designed to investigate mechanisms of
adenosine (
ADO)-mediated prolongation of conductivity through the atrioventricular (AV) node during
myocardial ischemia. Using the Langendorff preparation of the guinea pig heart, we tested the hypothesis that extracellular
potassium concentration elevated due to
ischemia could augment
ADO effect. Exposure of the heart preparation to either stop-flow or hypoxic
Krebs-Henseleit solution (KH) inhibited AV node conductivity observed as an increase in SH interval, and finally resulted in
AV block. Superficial
potassium concentration ([K+]s), recorded simultaneously increased in response to each stop-flow or
hypoxia. Application of 0.1 mM
BaCl2 markedly increased the SH interval, yet it did neither protect the heart from
hypoxia-evoked
AV block nor did it prevent
hypoxia-induced [K+]s elevation. Neither did perfusion of the myocardium with modified KH containing 8 mM K+ affect the hypoxic
AV block and [K+]s increase. The hypoxic effects were not affected by
adenosine A1 agonist N6-cyclopentyl-adenosine (CPA, 30 nM). In the presence of CPA, application of high-K+ KH, where
potassium was elevated to the value of hypoxic level, did not affect the SH interval. On the other hand,
adenosine deaminase (ADA, 4 U/ml) significantly attenuated the hypoxic
AV block. This indicated an involvement of endogenous
ADO. Yet, in the presence of both ADA and CPA, the application of the high-K+ KH did not affect the SH interval. We concluded that increased extracellular [K+], elevated due to
hypoxia, did not participate in the
hypoxia-induced
AV block mediated by
ADO.