Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Palma‐Rigo, Kesia; Jackson, Kristy L.; Davern, Pamela J.; Nguyen‐Huu, Thu‐Phuc; Elghozi, Jean‐Luc; Head, Geoffrey A.

doi:10.1097/hjh.0b013e32834bbb6b

Cited by 21 publications

(21 citation statements)

References 46 publications

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“…BPH/2J mice are a model of lifelong hypertension on a genetic basis and manifest some of the cardinal features of essential hypertension, i.e., neurohumoral dysfunction, sympathetic activation, cardiac hypertrophy, and kidney atrophy (58,59). Due to long-lasting hypertension, BPH/2J mice are valuable in hypertension research, akin to spontaneously hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension

Faraco¹,

Sugiyama²,

Lane³

et al. 2016

Journal of Clinical Investigation

270

358

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In this study we investigated the contribution of PVMs to the neurovascular and cognitive dysfunction induced by hypertension. We found that depletion of PVMs in models of chronic hypertension suppresses vascular oxidative stress and ameliorates the attendant impairment in neurovascular coupling and endothelium-dependent responses. Studies in bone marrow (BM) chimeras provided evidence that the dysfunction is mediated by ANGII acting on PVM AT1Rs resulting in NOX2-dependent ROS production. Importantly, concomitant to the neurovascular improvement, PVM depletion also rescued cognitive dysfunction. The findings unveil a previously unrecognized role of PVMs in the neurovascular and cognitive dysfunction induced by hypertension, and identify PVMs as a novel pathogenic component of the NVU of critical importance for brain health.

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Section: Discussionmentioning

confidence: 99%

Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension

Faraco¹,

Sugiyama²,

Lane³

et al. 2016

Journal of Clinical Investigation

270

358

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“…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%

“…This is based on the ability of the ganglion blocker pentolinium to abolish the blood pressure (BP) difference between normotensive BPN/3J and BPH/2J mice while blockade of the renin-angiotensin system had an equal hypotensive effect in both strains [2]. Thus, it is likely that there is a greater sympathetic contribution to the hypertension in BPH/2J mice.…”

Section: Introductionmentioning

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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“…This KD mouse displays a decrease in the release of ACh of 40% and 70%, respectively, for heterozygous and homozygous (HOM) individuals (55, 56). Due to its parasympathetic impairment, the VAChT KD HOM mouse model (31) may be quite useful for studying pathophysiological processes involving sympathovagal imbalance (22,23,50,62).It has also been demonstrated that individuals with several disorders affecting the autonomic nervous system and cardiac function, e.g., heart failure, myocardial infarction, diabetes, and hypertension, have loss of daily variations in cardiovascular parameters (1,7,21,37,54,74,77). Moreover, a decrease in heart rate (HR) variability (27) and baroreflex sensitivity (BRS) (51) as well as an exaggerated cardiovascular response to stress have been described under these pathological conditions (10,11,49) and associated with higher cardiovascular risk (13,78).…”

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confidence: 99%

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confidence: 99%

Autonomic cardiocirculatory control in mice with reduced expression of the vesicular acetylcholine transporter

Durand

Becari

Tezini

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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In cardiovascular diseases, sympathetic tone has been comprehensively studied, whereas parasympathetic tone has received minor attention. The vesicular ACh transporter (VAChT) knockdown homozygous (VAChT KD HOM ) mouse is a useful model for examining the cardiocirculatory sympathovagal balance. Therefore, we investigated whether cholinergic dysfunction caused by reduced VAChT expression could adversely impact hemodynamic parameter [arterial pressure (AP) and heart rate (HR)] daily oscillation, baroreflex sensitivity, hemodynamic variability, sympathovagal balance, and cardiovascular reactivity to restraint stress. Wild-type and VAChT KD HOM mice were anesthetized for telemetry transmitter implantation, and APs and HRs were recorded 10 days after surgical recovery. Changes in HR elicited by methylatropine and propranolol provided the indexes of sympathovagal tone. Cardiovascular reactivity in response to a restraint test was examined 24 h after continuous recordings of AP and HR. VAChT KD HOM mice exhibited reduced parasympathetic and elevated sympathetic tone. Daily oscillations of AP and HR as well as AP variability were similar between groups. Nevertheless, HR variability, patterns with two dissimilar variations from symbolic analysis, and baroreflex sensitivity were reduced in VAChT KD HOM mice. The change in mean AP due to restraint stress was greater in VAChT KD HOM mice, whereas the tachycardic response was not. These findings demonstrate that the cholinergic dysfunction present in the VAChT KD HOM mouse did not adversely impact basal hemodynamic parameters but promoted autonomic imbalance, an attenuation of baroreflex sensitivity, and a greater pressure response to restraint stress. These results provide a framework for understanding how autonomic imbalance impacts cardiovascular function. daily hemodynamic oscillations; heart rate variability; mice; parasympathetic nervous system; vesicular acetylcholine transporter IN A NUMBER of cardiovascular diseases, e.g., heart failure, one of the most important changes to maintain cardiac output is sympathetic overactivity (79). This outcome is accompanied by a reduction in parasympathetic tone (47). Derangement of the autonomic nervous system seems to contribute to cardiac dysfunction and remodeling (17). However, although control of sympathetic tone in cardiovascular diseases has been extensively studied, less attention has been given to the role played by parasympathetic function (47).Regulation of cholinergic activity in the heart has recently emerged as an important step in the preservation of long-term cardiac function (64). Indeed, recent epidemiological evidence suggests improved outcomes for cardiovascular diseases in patients with Alzheimer's disease receiving anticholinesterase treatment (40,46). In addition, studies using acetylcholinesterase inhibitors in animals and patients with heart failure have demonstrated that it may be potentially useful for cardiovascular protection, resulting in beneficial effects for markers of cardiovascular risk and dysfu...

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Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

Cited by 21 publications

References 46 publications

Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension

Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension

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

Autonomic cardiocirculatory control in mice with reduced expression of the vesicular acetylcholine transporter

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