Modulation of in situ canine intrinsic cardiac neuronal activity by locally applied adenosine, ATP, or analogues.

To determine whether adenosine or ATP can modify mammalian intrinsic cardiac neurons, these substances, as well as their analogues 5'-(N-ethylcarboxamido)-adenosine (NECA), N6-cyclopentyladenosine (CPA), and beta,gamma-methylene ATP (beta,gamma-mATP), were applied in microliter quantities adjacent to spontaneously active canine atrial ganglionated plexus neurons in 14 anesthetized open-chest dogs. Adenosine, NECA, and CPA induced neuronal responses, neuronal activity being either increased or decreased in 81, 86, and 86% of the sites tested, respectively. Cardiovascular responses were elicited by these agents in 21-31% of neurally active loci. ATP and beta,gamma-mATP elicited neuronal responses in 100 and 70% of tested loci, respectively. Associated cardiovascular responses were elicited by ATP and beta,gamma-mATP in 35 and 18% of the sites, respectively. After acute decentralization of the intrinsic cardiac nervous system, neuronal responses were elicited by purines in 73% of the previously active sites, while cardiovascular responses were either attenuated or eliminated. It is concluded that exogenous purine nucleosides and nucleotides can modulate the activity generated by in situ intrinsic cardiac neurons presumably by acting on P1 and P2 purinoreceptors. Furthermore, these data indicate that purine sensitive intrinsic cardiac neurons are involved in cardiac regulation.