['B-type natriuretic peptide (BNP)-natriuretic peptide receptor A (NPR-A) receptor signalling inhibits cardiac sympathetic neurotransmission, although C-type natriuretic peptide (CNP) is the predominant neuropeptide of the nervous system with expression in the heart and vasculature. We hypothesized that CNP acts similarly to BNP, and that transgenic rats (TGRs) with neuron-specific overexpression of a dominant negative NPR-B receptor would develop heightened sympathetic drive.', 'Mean arterial pressure and heart rate (HR) were significantly (P\u2009<\u20090.05) elevated in freely moving TGRs (n\u2009=\u20099) compared with Sprague Dawley (SD) controls (n\u2009=\u200910). TGR had impaired left ventricular systolic function and spectral analysis of HR variability suggested a shift towards sympathoexcitation. Immunohistochemistry demonstrated co-staining of NPR-B with tyrosine hydroxylase in stellate ganglia neurons. In SD rats, CNP (250\u2009nM, n\u2009=\u20098) significantly reduced the tachycardia during right stellate ganglion stimulation (1-7\u2009Hz) in vitro whereas the response to bath-applied norepinephrine (NE, 1\u2009μM, n\u2009=\u20096) remained intact. CNP (250\u2009nM, n\u2009=\u20098) significantly reduced the release of '] Does c-type natriuretic peptide and natriuretic peptide receptor B signalling inhibit cardiac sympathetic neurotransmission and autonomic function?