Peripheral chemoreceptor afferent signaling is crucial for mediating exercise training-induced resting bradycardia and blood pressure reduction via plasticity of paraventricular nucleus oxytocinergic neurons.
New findings What is the central question of this study? This study addresses the role of carotid chemoreceptors in mediating exercise training‐induced plasticity in the paraventricular nucleus and changes in heart rate and blood pressure in normotensive and hypertensive rats. What is the main finding and its importance? The present data show that peripheral chemoreceptor afferent signalling is crucial to drive the plasticity/activity of paraventricular nucleus oxytocinergic pre‐autonomic neurons, thus mediating training‐induced resting bradycardia in normotensive and hypertensive rats and pressure reduction in hypertensive animals. We showed previously that sino‐aortic denervation prevented training‐induced plasticity in pre‐autonomic oxytocinergic neurons and blocked the beneficial effects of training. In this study, we investigate the combined effect of training and removal of specific chemoreceptor afferents on both cardiovascular parameters and oxytocin (OT) gene and protein expression within the hypothalamic paraventricular nucleus (PVN). Wistar rats and spontaneously hypertensive rats (SHRs) underwent carotid body denervation or sham surgery and were trained or kept sedentary for 3 months. After haemodynamic measurements at rest, rats were anaesthetized for brain perfusion. Fresh (perfused with PBS) and fixed brains (perfused with 4% paraformaldehyde) were processed for PVN OT mRNA (real‐time PCR) and OT immunoreactivity within PVN subnuclei. In sham‐operated rats, training improved treadmill performance and reduced resting heart rate (Wistar, −8%; SHRs, −10%), with a reduction in blood pressure only in SHRs (−8%). Training was accompanied by increased PVN OT mRNA expression (twofold increase in sham‐operated SHRs) and peptide density in the posterior, ventromedial and dorsal cap PVN subnuclei (on average 70% increase in both strains), with significant correlations between OT content and training‐induced resting bradycardia in sham‐operated groups. Carotid body denervation did not interfere with the performance gain, abolished chemoreflex activation (without changing baroreflex control) and blocked training‐induced cardiovascular adaptations and training‐induced changes in PVN OT content in both strains. After carotid body denervation, there was no correlation between OT mRNA or OT immunoractivity and resting heart rate. The chronic absence of chemoreceptor inputs uncovers an unknown role of chemoreceptor signalling in driving the plasticity/activity of PVN oxytocinergic pre‐autonomic neurons, thus mediating training‐induced cardiovascular adaptive responses.
Cruz et al. (Wed,) studied this question.