MODULATION BY ADRENERGIC TRANSMITTERS OF THE EFFERENT FUNCTION OF CAPSAICIN-SENSITIVE NERVES IN CARDIAC TISSUE

In atrial preparations obtained from reserpine-pre-treated guinea-pigs, incubated in the presence of 1-mu-M atropine plus 1-mu-M CGP 20712A (a beta-1 blocking drug), a positive inotropic effect due to CGRP release from capsaicin-sensitive sensory neurons was induced by electrical field stimulation (EFS). This response was concentration-dependently reduced by noradrenaline (0.01-3-mu-M), neuropeptide Y (NPY, 3-300 nM) and adenosine triphosphate (ATP, 1-30-mu-M). On the other hand, the overflow of [H-3]-noradrenaline from sympathetic nerve terminals induced by EFS in isolated atria obtained from normal untreated animals was not modified in 10 nM calcitonin gene-related peptide (CGRP). Substance P (SP) and neurokinin A (NKA), at concentrations ranging from 0.01 to 1-mu-M did not affect the cardiac response to field stimulation of adrenergic terminals of atrial tissue. These findings demonstrate that all the co-transmitters stored in adrenergic nerve terminals have a modulatory role on the efferent function of cardiac capsaicin-sensitive sensory neurons, while cardiac adrenergic neurotransmission is not influenced by the peptidergic transmitters released from sensory neurons.