Non-adrenergic non-cholinergic (NANC) neural control of the atrial myocardium.
1. Current concepts in the regulation of atrial contractility by non-adrenergic non-cholinergic (NANC) sensory nerves are reviewed. 2. There is now evidence that in addition to sympathetic and parasympathetic innervation capsaicin-sensitive sensory nerves contribute to the local control of atrial contractility by releasing NANC transmitters, such as calcitonin gene-related peptide (CGRP). 3. Certain chemical and physical stimuli affect atrial contractility by inducing the release of CGRP from sensory nerves. In addition, as widely recognized for the sympathetic and vagal atrial innervation, NANC neurotransmission is under the inhibitory control of several endogenous modulators. 4. Cardioexcitatory actions of NANC neurotransmission on the atrial myocardium are considered. 5. Pharmacological modulation of NANC neurotransmission and functional evidence for cross-talk between NANC and sympathetic neurones are also discussed.
Rubino
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Department of Anatomy and Developmental Biology, University College London England.
D000818:Animals; D016275:Atrial Function; D001341:Autonomic Nervous System / Q000502:physiology*; D006321:Heart / Q000294:innervation* / Q000502:physiology; D006801:Humans; D009435:Synaptic Transmission / Q000502:physiology