scholarly journals Pregnancy and the endocrine regulation of the baroreceptor reflex

2010 ◽  
Vol 299 (2) ◽  
pp. R439-R451 ◽  
Author(s):  
Virginia L. Brooks ◽  
Roger A. L. Dampney ◽  
Cheryl M. Heesch
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ventrolateral Medulla ◽  
Endocrine Regulation ◽  
Nerve Activity ◽  
Baroreflex Function ◽  
Premotor Neurons ◽  
The Brain

The purpose of this review is to delineate the general features of endocrine regulation of the baroreceptor reflex, as well as specific contributions during pregnancy. In contrast to the programmed changes in baroreflex function that occur in situations initiated by central command (e.g., exercise or stress), the complex endocrine milieu often associated with physiological and pathophysiological states can influence the central baroreflex neuronal circuitry via multiple sites and mechanisms, thereby producing varied changes in baroreflex function. During pregnancy, baroreflex gain is markedly attenuated, and at least two hormonal mechanisms contribute, each at different brain sites: increased levels of the neurosteroid 3α-hydroxy-dihydroprogesterone (3α-OH-DHP), acting in the rostral ventrolateral medulla (RVLM), and reduced actions of insulin in the forebrain. 3α-OH-DHP appears to potentiate baroreflex-independent GABAergic inhibition of premotor neurons in the RVLM, which decreases the range of sympathetic nerve activity that can be elicited by changes in arterial pressure. In contrast, reductions in the levels or actions of insulin in the brain blunt baroreflex efferent responses to increments or decrements in arterial pressure. Although plasma levels of angiotensin II are increased in pregnancy, this is not responsible for the reduction in baroreflex gain, although it may contribute to the increased level of sympathetic nerve activity in this condition. How these different hormonal effects are integrated within the brain, as well as possible interactions with additional potential neuromodulators that influence baroreflex function during pregnancy and other physiological and pathophysiological states, remains to be clearly delineated.

PACAP is expressed in sympathoexcitatory bulbospinal C1 neurons of the brain stem and increases sympathetic nerve activity in vivo

2008 ◽  
Vol 294 (4) ◽  
pp. R1304-R1311 ◽  
Author(s):  
Melissa M. J. Farnham ◽  
Qun Li ◽  
Ann K. Goodchild ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Intrathecal Administration ◽  
Ventrolateral Medulla ◽  
Cell Group ◽  
Nerve Activity ◽  
The Brain

Pituitary adenylate cyclase-activating polypeptide (PACAP) is an excitatory neuropeptide present in the rat brain stem. The extent of its localization within catecholaminergic groups and bulbospinal sympathoexcitatory neurons is not established. Using immunohistochemistry and in situ hybridization, we determined the extent of any colocalization with catecholaminergic and/or bulbospinal projections from the brain stem was determined. PACAP mRNA was found in tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the C1-C3 cell groups. In the rostral ventrolateral medulla (RVLM), PACAP mRNA was found in 84% of the TH-ir neurons and 82% of bulbospinal TH-ir neurons. The functional significance of these PACAP mRNA positive bulbospinal neurons was tested by intrathecal administration of PACAP-38 in anaesthetized rats. Splanchnic sympathetic nerve activity doubled (110%) and heart rate rose significantly (19%), although blood pressure was unaffected. In addition, as previously reported, PACAP was found in the A1 cell group but not in the A5 cell group or in the locus coeruleus. The RVLM is the primary site responsible for the tonic and reflex control of blood pressure through the activity of bulbospinal presympathetic neurons, the majority of which contain TH. The results indicate 1) that pontomedullary neurons containing both TH and PACAP that project to the intermediolateral cell column originate from C1-C3 and not A5, and 2) intrathecal PACAP-38 causes a prolonged, sympathoexcitatory effect.

scholarly journals “Real-time” imaging of cortical and subcortical sites of cardiovascular control: concurrent recordings of sympathetic nerve activity and fMRI in awake subjects

2016 ◽  
Vol 116 (3) ◽  
pp. 1199-1207 ◽  
Author(s):  
Vaughan G. Macefield ◽  
Luke A. Henderson
Keyword(s):  
Orbitofrontal Cortex ◽  
Sympathetic Nerve ◽  
Signal Intensity ◽  
Sympathetic Nerve Activity ◽  
Human Subjects ◽  
Ventrolateral Medulla ◽  
Bold Signal ◽  
Nerve Activity ◽  
The Right ◽  
The Brain

We review our approach to functionally identifying cortical and subcortical areas involved in the generation of spontaneous fluctuations in sympathetic outflow to muscle or skin. We record muscle sympathetic nerve activity (MSNA) or skin sympathetic nerve activity (SSNA), via a tungsten microelectrode inserted percutaneously into the common peroneal nerve, at the same time as performing functional magnetic resonance imaging (fMRI) of the brain. By taking advantage of the neurovascular coupling delay associated with BOLD (blood oxygen level dependent) fMRI, and the delay associated with conduction of a burst of sympathetic impulses to the peripheral recording site, we can identify structures in which BOLD signal intensity covaries with MSNA or SSNA. Using this approach, we found MSNA-coupled increases in BOLD signal intensity in the mid-insula and dorsomedial hypothalamus on the left side, and in dorsolateral prefrontal cortex, posterior cingulate cortex, precuneus, ventromedial hypothalamus and rostral ventrolateral medulla on both sides. Conversely, spontaneous bursts of SSNA were positively correlated with BOLD signal intensity in the ventromedial thalamus and posterior insula on the left side, and in the anterior insula, orbitofrontal cortex and frontal cortex on the right side, and in the mid-cingulate cortex and precuneus on both sides. Inverse relationships were observed between MSNA and BOLD signal intensity in the right ventral insula, nucleus tractus solitarius and caudal ventrolateral medulla, and between SSNA and signal intensity in the left orbitofrontal cortex. These results emphasize the contributions of cortical regions of the brain to sympathetic outflow in awake human subjects, and the extensive interactions between cortical and subcortical regions in the ongoing regulation of sympathetic nerve activity to muscle and skin in awake human subjects.

Dorsomedial medulla is more susceptible than rostral ventrolateral medulla to hypoxic insult in cats

2001 ◽  
Vol 90 (1) ◽  
pp. 248-260 ◽  
Author(s):  
Ling-Zong Hong ◽  
Jon-Son Kuo ◽  
Mao-Hsiung Yen ◽  
Chok-Yung Chai
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Systemic Arterial Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Pressor Responses ◽  
Norepinephrine Depletion ◽  
Vertebral Nerve

We investigated the responses of systemic arterial pressure and vertebral sympathetic nerve activity to glutamate microinjections (0.1 M, 70 nl) in the dorsomedial (DM) and the rostral ventrolateral medulla (RVLM) before hypoxia and after reoxygenation (posthypoxia) after various degrees of hypoxia in anesthetized cats. Hypoxia was produced by ventilating 5% O2 and 95% N2 for different durations (hypoxia I-III). In intact cats, the glutamate-induced systemic arterial pressure and vertebral nerve activity responses of the DM were depressed after all degrees of hypoxia. Posthypoxic depression in the RVLM, however, was not observed until hypoxia II and III. Precollicular decerebration prevented depression in the RVLM, but, for the DM, it was effective only for hypoxia I. Baro- and chemoreceptor denervation abolished all posthypoxic depression in both the DM and the RVLM. Pressor responses to tyramine (100–400 μg/kg iv) remained unchanged after all degrees of hypoxia. These results suggest that the DM is more susceptible to hypoxia than the RVLM. The peripheral baro- and chemoreceptors and the suprapontine structures apparently play an important role in posthypoxic depression. Moreover, the depression is not due to the postganglionic norepinephrine depletion.

A neural set point for the long-term control of arterial pressure: beyond the arterial baroreceptor reflex

2005 ◽  
Vol 288 (4) ◽  
pp. R846-R855 ◽  
Author(s):  
John W. Osborn ◽  
Frédéric Jacob ◽  
Pilar Guzman
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Salt Intake ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Set Point ◽  
Arterial Baroreceptor Reflex ◽  
Arterial Baroreceptor

Arterial baroreceptor reflex control of renal sympathetic nerve activity (RSNA) has been proposed to play a role in long-term control of arterial pressure. The hypothesis that the “set point” of the acute RSNA baroreflex curve determines the long-term level of arterial pressure is presented and challenged. Contrary to the hypothesis, studies on the long-term effects of sinoaortic denervation (SAD) on arterial pressure and RSNA, as well as more recent studies of chronic baroreceptor “unloading” on arterial pressure, suggest that the basal levels of sympathetic nerve activity and arterial pressure are regulated independent of arterial baroreceptor input to the brainstem. Studies of the effect of SAD on the long-term salt sensitivity of arterial pressure are consistent with a short-term role, rather than a long-term role for the arterial baroreceptor reflex in regulation of arterial pressure during changes in dietary salt intake. Renal denervation studies suggest that renal nerves contribute to maintenance of the basal levels of arterial pressure. However, evidence that baroreflex control of the kidney plays a role in the maintenance of arterial pressure during changes in dietary salt intake is lacking. It is proposed that a “baroreflex-independent” sympathetic control system must exist for the long-term regulation of sympathetic nerve activity and arterial pressure. The concept of a central nervous system “set point” for long-term control of mean arterial pressure (CNS-MAP set point), and its involvement in the pathogenesis of hypertension, is discussed.

Exercise training attenuates increases in lumbar sympathetic nerve activity produced by stimulation of the rostral ventrolateral medulla

2007 ◽  
Vol 102 (2) ◽  
pp. 803-813 ◽  
Author(s):  
Patrick J. Mueller
Keyword(s):  
Nervous System ◽  
Mean Arterial Pressure ◽  
Exercise Training ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Sympathetic Nervous

Exercise training (ExTr) has been associated with blunted activation of the sympathetic nervous system in several animal models and in some human studies. Although these data are consistent with the hypothesis that ExTr reduces the incidence of cardiovascular diseases via reduced sympathoexcitation, the mechanisms are unknown. The rostral ventrolateral medulla (RVLM) is important in control of sympathetic nervous system activity in both physiological and pathophysiological states. The purpose of the present study was to test the hypothesis that ExTr results in reduced sympathoexcitation mediated at the level of the RVLM. Male Sprague-Dawley rats were treadmill trained or remained sedentary for 8–10 wk. RVLM microinjections were performed under Inactin anesthesia while mean arterial pressure, heart rate, and lumbar sympathetic nerve activity (LSNA) were recorded. Bilateral microinjections of the GABAA antagonist bicuculline (5 mM, 90 nl) into the RVLM increased LSNA in sedentary animals (169 ± 33%), which was blunted in ExTr animals (100 ± 22%, P < 0.05). Activation of the RVLM with unilateral microinjections of glutamate (10 mM, 30 nl) increased LSNA in sedentary animals (76 ± 13%), which was also attenuated by training (26 ± 2%, P < 0.05). Bilateral microinjections of the ionotropic glutamate receptor antagonist kynurenate (40 mM, 90 nl) produced small increases in mean arterial pressure and LSNA that were similar between groups. Results suggest that ExTr may reduce increases in LSNA due to reduced activation of the RVLM. Conversely, we speculate that the relatively enhanced activation of LSNA in sedentary animals may be related to the increased incidence of cardiovascular disease associated with a sedentary lifestyle.

Galanin microinjection into rostral ventrolateral medulla of the rat is hypotensive and attenuates sympathetic chemoreflex

2009 ◽  
Vol 296 (4) ◽  
pp. R1019-R1026 ◽  
Author(s):  
Stephen B. G. Abbott ◽  
Paul M. Pilowsky
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Somatosympathetic Reflex

Galanin is present in neurons in the brain that are important in the control of arterial pressure, and intracisternal administration of galanin evokes hypotension, but the site of action is unknown. In urethane-anesthetized, vagotomized mechanically ventilated Sprague-Dawley rats ( n = 34), we investigated the effects of microinjecting galanin (1 mM, 50 nl, 50 pmol) into the rostral ventrolateral medulla on resting splanchnic sympathetic nerve activity, arterial pressure, heart rate, and phrenic nerve activity. Second, we determined the effect of microinjecting galanin into the rostral ventrolateral medulla on the cardiovascular response to stimulation of central and peripheral chemoreceptors, arterial baroreceptors, and the somatosympathetic reflex. Galanin caused a prolonged reduction in resting splanchnic sympathetic nerve activity (−37.0 ± 7.2% of baseline), mean arterial pressure (−17.0 ± 3.5 mmHg), and heart rate (−25.0 ± 9.1 beats/min). Galanin increased the sympathoinhibitory response to aortic depressor nerve stimulation by 51.8%, had no effect on the somatosympathetic reflex, and markedly attenuated the effect of hypercapnia and hypoxia on arterial pressure (by 65% and 92.4% of control, respectively). These results suggest a role for galanin neurotransmission in the integration of the cardiovascular responses to hypoxia, hypercapnia, and the sympathetic baroreflex in the rostral ventrolateral medulla. The data suggest that galanin may be an important peptide in the homeostatic regulation of chemosensory reflexes.

Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM

2012 ◽  
Vol 302 (3) ◽  
pp. R365-R372 ◽  
Author(s):  
Andrea H. Gaede ◽  
Paul M. Pilowsky
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Phrenic Nerve ◽  
Sympathetic Nerve ◽  
Chromogranin A ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Cardiorespiratory Control

Hypertension is a major cause of morbidity. The neuropeptide catestatin [human chromogranin A-(352–372)] is a peptide product of the vesicular protein chromogranin A. Studies in the periphery and in vitro studies show that catestatin blocks nicotine-stimulated catecholamine release and interacts with β-adrenoceptors and histamine receptors. Catestatin immunoreactivity is present in the rostral ventrolateral medulla (RVLM), a key site for blood pressure control in the brain stem. Recently, we reported that microinjection of catestatin into the RVLM is sympathoexcitatory and increases barosensitivity. Here, we report the effects of microinjection of catestatin (1 mM, 50 nl) into the caudal ventrolateral medulla (CVLM) in urethane-anesthetized, bilaterally vagotomized, artificially ventilated Sprague-Dawley rats ( n = 8). We recorded resting arterial pressure, splanchnic sympathetic nerve activity, phrenic nerve activity, heart rate, and measured cardiovascular homeostatic reflexes. Homeostatic reflexes were evaluated by measuring cardiovascular responses to carotid baroreceptor and peripheral chemoreceptor activation. Catestatin decreased basal levels of arterial pressure (−23 ± 4 mmHg), sympathetic nerve activity (-26.6 ± 5.7%), heart rate (−19 ± 5 bpm), and phrenic nerve amplitude (−16.8 ± 3.3%). Catestatin caused a 15% decrease in phrenic inspiratory period (Ti) and a 16% increase in phrenic expiratory period (Te) but had no net effect on the phrenic interburst interval (Ttot). Catestatin decreased sympathetic barosensitivity by 63.6% and attenuated the peripheral chemoreflex (sympathetic nerve response to brief hypoxia; range decreased 39.9%; slope decreased 30.1%). The results suggest that catestatin plays an important role in central cardiorespiratory control.

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