Activation of lateral parabrachial nucleus neurons restores blood pressure and sympathetic vasomotor drive after hypotensive hemorrhage

Blair, Martha L.; Mickelsen, Deanne

doi:10.1152/ajpregu.00049.2006

Cited by 11 publications

(11 citation statements)

References 49 publications

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“…In the present study, HEM was shown to induce a significant increase in FLI in the external subnucleus of the LPBN in SED animals, supporting previous findings that correlate neural activation within the external LPBN with spontaneous recovery following HEM (Blair, Jaworski et al 2001; Blair and Mickelsen 2006). Somewhat unexpected however, FLI in the LPBN of the EX group following HEM was not identified to be significant different from the CON group in most subnuclei of the LPBN examined, with the exception of the central lateral subnucleus of the rostral LPBN.…”

Section: Discussionsupporting

confidence: 92%

“…Central activation of the parabrachial nucleus (Ward 1989; Blair, Jaworski et al 2001; Blair and Mickelsen 2006), more specifically, the external subnucleus in the ventrolateral region of the LPBN, has been implicated in both central modulation of baroreflex function (Saleh and Connell 1997; Len and Chan 1999; Len and Chan 2001; Wei 2008) and the recovery from HEM. In the present study, HEM was shown to induce a significant increase in FLI in the external subnucleus of the LPBN in SED animals, supporting previous findings that correlate neural activation within the external LPBN with spontaneous recovery following HEM (Blair, Jaworski et al 2001; Blair and Mickelsen 2006).…”

Section: Discussionmentioning

confidence: 99%

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Daily voluntary exercise alters the cardiovascular response to hemorrhage in conscious male rats

Ahlgren

Hayward

2011

Autonomic Neuroscience

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The present study tested the hypothesis that voluntary wheel-exercised rats would better tolerate severe hemorrhage (HEM) compared to age matched sedentary (SED) controls. Conscious rats housed with (EX, n=8) or without (SED, n=8) a running wheel for 6 weeks underwent a 30% total blood volume HEM over 15 min. and were euthanized 90 min later and brain tissue processed for Fos-like immunoreactivity (FLI). Both EX and SED groups displayed typical responses to HEM (initial tachycardia followed by decreased HR and MAP) but at the end of HEM, mean arterial pressure (93±6 vs 58±3 mmHg) and heart rate (316±17 vs. 247±22 bpm,) were higher in the EX vs. SED animals and 60 min following the end of HEM HR remained significantly elevated in the EX vs SED animals. The altered HR response to HEM in the EX animals was linked to a significant difference in sympathovagal drive identified by heart rate variability analysis and an augmented baroreflex response to hypotension tested in a separate group of animals (n=4–5/group). In many of the brain regions analyzed EX rats displayed lower levels of FLI compared to SED rats. Significantly lower levels of FLI in the EX vs SED rats were identified in the middle and caudal external lateral subnucleus of the lateral parabrachial nucleus and the dorsal cap of the hypothalamic paraventricular nucleus. These results suggest that enhanced tolerance to HEM following daily exercise may result from EX-induced reduced excitation or exaggerated inhibition in central circuits involved in autonomic control.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Daily voluntary exercise alters the cardiovascular response to hemorrhage in conscious male rats

Ahlgren

Hayward

2011

Autonomic Neuroscience

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“…Two previous studies have evaluated the effect of atropine administration on MAP in the conscious rat. Interestingly, the study that utilized hemorrhage rates closer to 1 mg/kg/min reported no effect of atropine administration on MAP (4). Alternatively the other study utilizing a faster rate of blood loss (∼2.2.ml/kg/min) demonstrated a significant elevation of MAP following parasympathetic blockade and severe hemorrhage (25).…”

Section: 1 Discussionmentioning

confidence: 99%

Modulation of heart rate variability during severe hemorrhage at different rates in conscious rats

Porter

Ahlgren

Stanley

et al. 2009

Autonomic Neuroscience

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This study was undertaken to evaluate heart rate (HR) regulation during severe hemorrhage (HEM) at different rates of blood loss. Chronically instrumented male rats underwent HEM at one of three rates: slow (0.5 ml/min/kg; S-HEM), intermediate (1.0 ml/min/kg I-HEM), or 2.0 ml/min/kg (fast; F-HEM) until 30% of the estimated total blood volume (ETBV) was withdrawn. Heart rate variability analysis was performed and the absolute power within the low frequency (LF; 0.16-0.6 Hz) and high frequency (HF; 0.6 -3 Hz) ranges were evaluated. During the first 15% of ETBV loss, arterial pressure (AP) was maintained while HR increased. The increase in HR was greatest in the S-HEM and I-HEM groups and was associated with a significant reduction in HF power in the S-HEM group only. As blood loss progressed AP and HR declined in all treatment groups. The decrease in HR was associated with a significant increase in HF power in the F-HEM and I-HEM groups only. Parasympathetic blockade with atropine methyl bromide eliminated all decreases in HR, independent of rate of hemorrhage. Blockade of parasympathetic activity also significantly increased the AP at ETBV losses ≥20% independent of the rate of hemorrhage. The effect of atropine on AP was most noticeable in the S-HEM and F-HEM groups. These results demonstrate that rate of blood loss has an important impact on autonomic regulation during severe HEM and support previous findings that neural strategies underlying autonomic control may vary depending on the rate of blood loss.

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“…The analysis that was used was a modification of the method used by Blair and Mickelsen (5). Briefly, the standards were made with 1% plasma at 0, 1, 5, 10, and 20 g/ml of Evan's blue dye.…”

Section: Animals and Experiments Animals Were Housed In The Virginiamentioning

confidence: 99%

Increased renal α-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy

West

Zhang

Ecker

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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West C, Zhang Z, Ecker G, Masilamani SM. Increased renal ␣-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy. Am J Physiol Regul Integr Comp Physiol 299: R1326 -R1332, 2010. First published August 4, 2010 doi:10.1152/ajpregu.00082.2010.-Pregnancy-mediated sodium (Na) retention is required to provide an increase in plasma volume for the growing fetus. The mechanisms responsible for this Na retention are not clear. We first used a targeted proteomics approach and found that there were no changes in the protein abundance compared with virgin rats of the ␤ or ␥ ENaC, type 3 Na ϩ /H ϩ exchanger (NHE3), bumetanide-sensitive cotransporter (NKCC2), or NaCl cotransporter (NCC) in mid-or late pregnancy. In contrast, we observed marked increases in the abundance of the ␣-ENaC subunit. The plasma volume increased progressively during pregnancy with the greatest plasma volume being evident in late pregnancy. ENaC inhibition abolished the difference in plasma volume status between virgin and pregnant rats. To determine the in vivo activity of ENaC, we conducted in vivo studies of rats in late pregnancy (days 18 -20) and virgin rats to measure the natriuretic response to ENaC blockade (with benzamil). The in vivo activity of ENaC (UNaV postbenzamil-UNaV postvehicle) was markedly increased in late pregnancy, and this difference was abolished by pretreatment with the mineralocorticoid receptor antagonist, eplerenone. These findings demonstrate that the increased ␣-ENaC subunit of pregnancy is associated with an mineralocorticoid-dependent increase in ENaC activity. Further, we show that ENaC activity is a major contributor of plasma volume status in late pregnancy. These changes are likely to contribute to the renal sodium retention and plasma volume expansion required for an optimal pregnancy. collecting duct; plasma volume expansion; sodium retention IN HUMANS AND RATS, PREGNANCY is accompanied by marked changes in cardiovascular function, renal function, and fluid homeostasis. These adaptations permit an increase in blood volume that will supply the growing uterus and fetus without the development of maternal hypertension.A normal healthy pregnancy is associated with a cumulative plasma volume expansion (PVE) (30 -50%) and avid sodium retention (2,26,27). Failure of this adaptation is associated with maternal morbidity/mortality and intrauterine growth restriction (3, 27). Despite the progressive PVE, there is no increase in maternal blood pressure due to a marked decrease in total peripheral vascular resistance (2, 7).Renal sodium excretion determines volume homeostasis and the progressive PVE of normal pregnancy must reflect net renal sodium retention. Alexander et al.(1) performed balance studies in the pregnant rat that demonstrated cumulative sodium retention during pregnancy. The reabsorption of sodium along the renal tubule is determined by the regulation of the individual tubular cotransporters and channels (16), such that a change in the activity of any transporter or channel...

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Activation of lateral parabrachial nucleus neurons restores blood pressure and sympathetic vasomotor drive after hypotensive hemorrhage

Cited by 11 publications

References 49 publications

Daily voluntary exercise alters the cardiovascular response to hemorrhage in conscious male rats

Daily voluntary exercise alters the cardiovascular response to hemorrhage in conscious male rats

Modulation of heart rate variability during severe hemorrhage at different rates in conscious rats

Increased renal α-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy

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