Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress

Chen, Daian; Jancovski, Nikola; Bassi, Jaspreet K; Nguyen-Huu, Thu Phuc; Choong, Yan Ting; Palma‐Rigo, Kesia; Davern, Pamela J.; Gurley, Susan B.; Thomas, Walter G.; Head, Geoffrey A.; Allen, Andrew M.

doi:10.1523/jneurosci.5360-11.2012

Cited by 41 publications

(39 citation statements)

References 53 publications

(60 reference statements)

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“…Consistent with this possibility the RVLM seems hyperreactive to angiotensin II in several hypertension models (9,83). This last evidence implicates the C1 cells perhaps more directly in the pathological process because, in the RVLM, angiotensin-1A receptors (AT1R) are predominantly expressed by these neurons (34).…”

Section: C1 Cells and Diseasementioning

confidence: 62%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

248

262

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The C1 neurons reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM, IVLM). They use glutamate as a fast transmitter and synthesize catecholamines plus various neuropeptides. These neurons regulate the hypothalamic pituitary axis via direct projections to the paraventricular nucleus and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. The presympathetic C1 cells, located in the RVLM, are probably organized in a roughly viscerotopic manner and most of them regulate the circulation. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception, and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brain stem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, subsets of C1 cells appear to be differentially recruited by pain, hypoxia, infection/inflammation, hemorrhage, and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic, and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension, and blood loss. C1 cells may also contribute to glucose and cardiovascular homeostasis in the absence of such physical stresses, and C1 cell hyperactivity may contribute to the increase in sympathetic nerve activity associated with diseases such as hypertension. C1 neurons; blood pressure; brain stem BEST KNOWN for their contribution to the control of arterial pressure (AP), the C1 neurons have also been implicated in many other physiological processes ranging from neuroendocrine responses to infection and inflammation, glucose homeostasis, reproduction, breathing, thermoregulation, hypothalamo-pituitary axis (HPA)-mediated stress responses, and food consumption. The purpose of this review is to summarize the most salient information concerning the C1 cells, to point out some of the remaining gaps in our current knowledge, and to suggest a few unifying physiological principles that could account for these seemingly disparate observations. Based on the various effects attributed to the C1 cells and what is currently known of their synaptic inputs, we propose that these neurons are, figuratively speaking, the body's "emergency medical technicians." By this we imply that these neurons produce stereotyped autonomic, metabolic, and neuroendocrine responses designed to help the organism survive major acute physical stresses such as accidental, pathological, or dive-related hypoxia or physical injury and its associated cohort of acute infection, blood loss, and hypotension. These emergency responses include, in the short term and depending on the stress, vasoconstriction, cardioinhibition, or acceleration, breathing stimulation, antidiuresis, changes in metabolism, and gastrointestinal (GI) functions designed to conserve pe...

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Section: C1 Cells and Diseasementioning

confidence: 62%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

248

262

View full text Add to dashboard Cite

show abstract

“…Restraint stress involved guiding the mouse into a cylindrical Plexi glass restrainer with a sliding back plate to confine the mouse without applying physical pressure. More detail is provided in previous publications [1,2,4,5,[22][23][24].…”

Section: Assessment Of Cardiovascular Reactivity In Response To Stresmentioning

confidence: 99%

“…The auto-power and cross-power spectra were calculated for multiple overlapping (by 50%) segments of MAP and HR using a fast Fourier transform as adapted for conscious mice [22]. The cardiac baroreflex sensitivity was estimated as the average value of the transfer gain in the frequency band between 0.3 and 0.5 Hz [22]. Baroreflex slope was considered significant if the coherence between MAP and HR across several overlapping segments in the analyzed frequency band was more than 0.4.…”

Section: Cardiovascular Variability and Cardiac Baroreceptor Sensitivitymentioning

confidence: 99%

GABAA receptor dysfunction contributes to high blood pressure and exaggerated response to stress in Schlager genetically hypertensive mice

Davern

Chowdhury

Jackson

et al. 2014

Journal of Hypertension

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“…Further investigations have found that NO,45 IL‐6,25 and corticotrophin‐releasing hormone and activation of the hypothalamic‐pituitary‐adrenal axis46 are directly involved in the physiological responses to CSS. The renin‐angiotensin system plays a complex role in the pressor response to CSS, with AT 1A receptors having both prohypertensive and antihypertensive roles, depending on their location 3, 33, 34, 47, 48, 49. Future research is needed to determine whether endothelium‐derived ET‐1 interacts with these other pathways or vice versa to mediate the acute pressor response.…”

Section: Discussionmentioning

confidence: 99%

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

Fox

Becker

Loria

et al. 2018

JAHA

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BackgroundAcute psychosocial stress provokes increases in circulating endothelin‐1 (ET‐1) levels in humans and animal models. However, key questions about the physiological function and cellular source of stress‐induced ET‐1 remain unanswered. We hypothesized that endothelium‐derived ET‐1 contributes to the acute pressor response to stress via activation of the endothelin A receptor.Methods and ResultsAdult male vascular endothelium‐specific ET‐1 knockout mice and control mice that were homozygous for the floxed allele were exposed to acute psychosocial stress in the form of cage switch stress (CSS), with blood pressure measured by telemetry. An acute pressor response was elicited by CSS in both genotypes; however, this response was significantly blunted in vascular endothelium‐specific ET‐1 knockout mice compared with control mice that were homozygous for the floxed allele. In mice pretreated for 3 days with the endothelin A antagonist, ABT‐627, or the dual endothelin A/B receptor antagonist, A‐182086, the pressor response to CSS was similar between genotypes. CSS significantly increased plasma ET‐1 levels in control mice that were homozygous for the floxed allele. CSS failed to elicit an increase in plasma ET‐1 in vascular endothelium‐specific ET‐1 knockout mice. Telemetry frequency domain analyses suggested similar autonomic responses to stress between genotypes, and isolated resistance arteries demonstrated similar sensitivity to α1‐adrenergic receptor‐mediated vasoconstriction.ConclusionsThese findings specify that acute stress‐induced activation of endothelium‐derived ET‐1 and subsequent endothelin A receptor activation is a novel mediator of the blood pressure response to acute psychosocial stress.

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Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress

Cited by 41 publications

References 53 publications

C1 neurons: the body's EMTs

C1 neurons: the body's EMTs

GABAA receptor dysfunction contributes to high blood pressure and exaggerated response to stress in Schlager genetically hypertensive mice

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium‐Derived Endothelin‐1

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