Medullary Respiratory Network Drives Sympathetic Overactivity and Hypertension in Rats Submitted to Chronic Intermittent Hypoxia

Prenatal stress-induced alterations in major physiological systems correlate with gut microbiota composition in adulthood

“…Remarkably, neurogenic shift of the arterial pressure 'set-point' via enhanced sympathetic drive can be involved in the pathogenesis of essential hypertension (Mancia et al, 1999;Osborn, 2005). Of note, elevated blood pressure has been linked to aberrant respiratory-sympathetic coupling in the brainstem (Moraes et al, 2012), which is interesting in the context of our observation of increased breathing variability in PNS rats (Suppl. Table 1).…”

Respiratory Network Enhances the Sympathoinhibitory Component of Baroreflex of Rats Submitted to Chronic Intermittent Hypoxia

“…Therefore, this study provides a foundation for more focused exploration of CIH-induced changes in central respiratory-sympathetic coupling as a potential mechanism underlying the onset of sympathetic overactivity and hypertension in rats. 3,4,9 The cellular and molecular mechanisms underlying this changed coupling between sympathetic and respiratory activities observed after CIH exposure are currently under investigation in our laboratory.…”

“…[1][2][3][4] The CIH-induced hypertension in rats can be prevented by sympathetic nerve chemical denervation, renal sympathectomy, and adrenal medullectomy. 1,5,6 Rats submitted to CIH also presented a larger fall in arterial pressure in response to ganglionic blockade and augmented power of oscillatory components at low and high frequencies in systolic arterial pressure.…”

“…In spite of some advances in our understanding of baroreflex function in rats after CIH, little is currently known about the functional changes in the sympathoinhibitory component of baroreflex induced by CIH and associated plasticity in the central pathways of the baroreflex. Considering that (1) respiratory modulation represents an important mechanism for control of RVLM presympathetic and CVLM GABAergic neurons and consequently the sympathetic outflow, [10][11][12]14 (2) CIH increases the central respiratory modulation of RVLM presympathetic neurons and sympathetic outflow, 3,4,9 and (3) respiration alters the sympathoinhibitory component of baroreflex 20,21 ; in this study, we hypothesized that changes in the respiratory network induced by CIH also reduce the sympathoinhibitory component of baroreflex and contribute to the development of hypertension. The data of this study performed in in situ preparations of rats demonstrate that 10 days of CIH enhanced the respiratory-related sympathoinhibitory component of baroreflex by increasing the expiratory baroreceptor inputs, probably through CVLM GABAergic neurons, to the respiratory-modulated RVLM presympathetic neurons.…”

The nucleus of the solitary tract and the coordination of respiratory and sympathetic activities

“…Recordings of parasympathetic and sympathetic nerves supplying the heart and blood vessels indicate that the autonomic activity controlling cardiac output and vascular resistance displays robust patterns of discharge entrained with the respiratory cycle (Adrian et al, 1932; Malpas, 1998; Barman and Gebber, 2000; Bouairi et al, 2004; Gilbey, 2007; Grossman and Taylor, 2007). As a consequence, the respiratory-related modulation of cardiovascular parasympathetic and sympathetic activities produces rhythmical oscillations in baseline heart rate (respiratory sinus arrhythmia) and arterial pressure levels (Traube-Hering waves) (Moraes et al, 2012b). The pattern of respiratory modulation of autonomic activity modifies according to the metabolic demand (blood gas changes, for instance) and contributes to generate appropriate respiratory and cardiovascular reflex responses (Dick et al, 2004; Molkov et al, 2011).…”