natriuretic-peptide--c-type and Tachycardia--Ventricular

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.. C-type natriuretic peptide reduces cardiac sympathetic neurotransmission via a reduction in neuronal calcium signalling and NE release through the NPR-B receptor. Situations impairing CNP-NPR-B signalling lead to hypertension, tachycardia, and impaired left ventricular systolic function secondary to sympatho-excitation.

Topics: Animals; Arterial Pressure; Calcium Signaling; Genetic Predisposition to Disease; Heart; Heart Rate; Hypertension; Natriuretic Peptide, C-Type; Norepinephrine; Phenotype; Rats, Sprague-Dawley; Rats, Transgenic; Receptors, Atrial Natriuretic Factor; Stellate Ganglion; Sympathetic Nervous System; Synaptic Transmission; Systole; Tachycardia, Ventricular; Time Factors; Tyrosine 3-Monooxygenase; Ventricular Dysfunction, Left; Ventricular Function, Left