MODULATION OF IN-SITU CANINE INTRINSIC CARDIAC NEURONAL-ACTIVITY BY LOCALLY APPLIED ADENOSINE, ATP, OR ANALOGS

To determine whether adenosine or ATP can modify mammalian intrinsic c ardiac neurons, these substances, as well as their analogues 5'-(N-eth ylcarboxamido)-adenosine (NECA), N6-cyclopentyladenosine (CPA), and be ta,gamma-methylene ATP (beta,gamma-mATP), were applied in micro-liter quantities adjacent to spontaneously active canine atrial ganglionated plexus neurons in 14 anesthetized open-chest dogs. Adenosine, NECA, a nd CPA induced neuronal responses, neuronal activity being either incr eased or decreased in 81, 86, and 86% of the sites tested, respectivel y. Cardiovascular responses were elicited by these agents in 21-31% of neurally active loci. ATP and beta,gamma-mATP elicited neuronal respo nses in 100 and 70% of tested loci, respectively. Associated cardiovas cular responses were elicited by ATP and beta,gamma-mATP in 35 and 18% of the sites, respectively. After acute decentralization of the intri nsic cardiac nervous system, neuronal responses were elicited by purin es in 73% of the previously active sites, while cardiovascular respons es were either attenuated or eliminated. It is concluded that exogenou s purine nucleosides and nucleotides can modulate the activity generat ed by in situ intrinsic cardiac neurons presumably by acting on P1 and P2 purinoreceptors. Furthermore, these data indicate that purine sens itive intrinsic cardiac neurons are involved in cardiac regulation.