The functional significance of neuropeptides and neurohormones throughout the neuroaxis has been the focus of considerable research over the past 25 years. These “gut peptides” or “reproductive hormones” have been localized within nuclei responsible for the relay of visceral afferent information to the forebrain. The presence of peptides and hormones along the gut- or heart-brain continuum suggests that these neurochemicals do more than modulate the visceral processes of digestion and reproduction respectively. Numerous studies have shown that the exogenous administration of these neurochemicals directly into visceral afferent nuclei significantly alters blood pressure, heart rate, autonomic tone and the sensitivity of the baroreceptor reflex (an index of sympatho-vagal balance). A strong inverse correlation has been demonstrated between the sensitivity of the baroreceptor reflex and susceptibility to lethal cardiac arrhythmias which lead ultimately to sudden cardiac death. The differential effects of various neurochemicals on the sensitivity of the baroreceptor reflex suggests that some neurochemicals may act as preventatives while others may actually contribute to the pathogenesis of neurogenic cardiac arrhythmias. Hormones such as estrogen, in addition to their neuroprotective properties, may also play a role in modulating the cardiovascular consequences to neurogenic pathologies including stroke and epilepsy. This review will summarize the evidence available which suggests that neuropeptides and neurohormones can alter both neurogenic as well as visceral pathology-induced changes in autonomic function resulting in an increased risk of sudden cardiac death.
Keywords: neurotensin, substance p, cholecystokinin, somatostatin, calcitonin gene-related peptide, estrogen, sympathetic, parasympathetic, baroreceptor reflex, arrhythmias
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