Heat acclimation affects the neuromodulatory role of AngII and nitric oxide during combined heat and hypohydration stress

Schwimmer, Hagit; Gerstberger, R.; Horowitz, Michal

doi:10.1016/j.molbrainres.2004.07.011

Cited by 23 publications

(39 citation statements)

References 24 publications

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“…With all the benefits acquired with the acclimation to heat, it seems, however, that all of them are lost with hypohydration. The endurance under heat of heat-acclimated rats is similar to those with no acclimation (Schwimmer et al 2004a).…”

Section: Combination Of Two Stresses: Heat and Hypohydrationmentioning

confidence: 67%

Physiological adaptations of small mammals to desert ecosystems

Schwimmer

Haim

2009

Integrative Zoology

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Adaptations of animals to the xeric environment have been studied in various taxonomic groups and across several deserts. Despite the impressive data that have been accumulated, the focus in most of these studies is mainly on the significance of one variable at a time. Here, we attempt to integrate between responses of several physiological systems, challenged by increasing diet and water salinity and extreme temperatures, acquired in different studies of thermo and osmo-regulatory adaptations, of small rodents, to the xeric environment. Studies have shown differential thermoregulatory responses to increased dietary salinity, which were attributed to habitat and habits of the relevant species. In the thermoregulatory studies, a potential adaptive significance of low metabolic rate was demonstrated. From an evolutionary point of view, the most important adaptation is in the timing of reproduction, as it enables the transfer of genetic properties to the next generation in an unpredictable ecosystem, where reproduction might not occur every year. Results in this aspect show that increased dietary salinity, through an increase in vasopressin plasma levels, plays an important role as a regulator of the reproductive system. We assume that the amount of food existing in the habitat and the amount of reserves in the animal in the form of white adipose tissue are important for reproduction. Photoperiod affects all studied physiological responses, emphasizing the importance of pre-acclimation to seasonal characteristics. We summarize the existing data and suggest neuro-endocrine pathways, which have a central role in these adaptations by affecting thermoregulation, osmoregulation and reproduction to create the optimal response to xeric conditions. These hypotheses can be used as the basis for future studies.

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Section: Combination Of Two Stresses: Heat and Hypohydrationmentioning

confidence: 67%

Physiological adaptations of small mammals to desert ecosystems

Schwimmer

Haim

2009

Integrative Zoology

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“…(77). Interestingly, there is evidence that the final shaping of AngII receptor signaling depends on cross-talk between nNOS [another thermal neuromodulator (55)] and AngII receptors at both transcriptional and posttranslational levels, including changes in receptor affinity and density and nNOS enzyme activity (196).…”

Section: Acclimation Neuroplasticity-pharmacological Approachmentioning

confidence: 99%

Heat Acclimation, Epigenetics, and Cytoprotection Memory

Horowitz

2014

Comprehensive Physiology

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Heat acclimation is a within-life phenotypic adaptation to heat. Plasticity of the thermoregulatory system is crucial for the induction of heat acclimation. In the last two decades, it has become clear that heat causes adaptive shifts in gene expression which adjust the protein balance. These changes are part of the evolvement of the acclimated phenotype. The molecular-cellular aspects of some acclimatory mechanisms that have only been explained by physiological-effectorial mechanisms have been discovered. This review attempts to bridge the gap between the classic physiological heat acclimation profile and the molecular/cellular mechanisms underlying the evolvement of the acclimated phenotype. Heat acclimation leads to leftward and rightward shifts in temperature thresholds of heat dissipation organs and thermal injury, respectively, thereby expanding the acclimated dynamic thermoregulatory range. Interactions between ambient temperature and afferent drives from effector organs to the hypothalamic thermoregulatory center with modifications in warm/cold sensitive neuron ratio and excitability contribute to the threshold changes. The altered threshold for thermal injury is associated with progressive enhancement of inducible cytoprotective networks, including HSP70, HSF1, and HIF-1ɑ. These molecules are also important in acclimatory kinetics. Aspects of cross-adaption, cross-tolerance and interference with heat acclimation are explained using molecular-cellular physiological interactions, with the heart, skeletal muscles, and water secretory glands as models. Lastly, the roles of epigenetic mechanisms in transcriptional regulation during induction of the acclimated phenotype, its decay, and reinduction are discussed. Posttranslational histone modifications in the promoters of hsp70 and hsp90 form part of our prototype model of heat-acclimation-mediated cytoprotective memory.

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“…4,8,11,12 Furthermore, it was recently suggested that AT 2 mediates HIF-1a upregulation, a key factor in HA-mediated neuroprotection. 1,13 The observation that the increase in hypothalamic AT 2 after HA 14 coincides with increased hypothalamic neurogenesis 15 may imply that AT 2 upregulation is one of the HA-induced changes that contribute to the orchestrated neuroprotective mechanisms. As some neuroprotective cellular downstream pathways of AT 2 are also upregulated in HA (e.g., Akt, HIF-1a, and BDNF), we aim to determine whether AT 2 is involved in the development of HA-mediated neuroprotection after TBI, which will promote its relevance as a drug target to confer neuroprotection and regeneration after TBI.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection after Traumatic Brain Injury in Heat-Acclimated Mice Involves Induced Neurogenesis and Activation of Angiotensin Receptor Type 2 Signaling

Umschweif

Shabashov²,

Alexandrovich³

et al. 2014

J Cereb Blood Flow Metab

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Long-term exposure of mice to mild heat (341C±11C) confers neuroprotection against traumatic brain injury (TBI); however, the underling mechanisms are not fully understood. Heat acclimation (HA) increases hypothalamic angiotensin II receptor type 2 (AT 2 ) expression and hypothalamic neurogenesis. Accumulating data suggest that activation of the brain AT 2 receptor confers protection against several types of brain pathologies, including ischemia, a hallmark of the secondary injury occurring following TBI. As AT 2 activates the same pro-survival pathways involved in HA-mediated neuroprotection (e.g., Akt phosphorylation, hypoxia-inducible factor 1a (HIF-1a), and brain-derived neurotrophic factor (BDNF)), we examined the role of AT 2 in HA-mediated neuroprotection after TBI. Using an AT 2 -specific antagonist PD123319, we found that the improvements in motor and cognitive recovery as well as reduced lesion volume and neurogenesis seen in HA mice were all diminished by AT 2 inhibition, whereas no significant alternations were observed in control mice. We also found that nerve growth factor/tropomyosin-related kinase receptor A (TrkA), BDNF/TrkB, and HIF-1a pathways are upregulated by HA and inhibited on PD123319 administration, suggesting that these pathways play a role in AT 2 signaling in HA mice. In conclusion, AT 2 is involved in HA-mediated neuroprotection, and AT 2 activation may be protective and should be considered a novel drug target in the treatment of TBI patients.

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Heat acclimation affects the neuromodulatory role of AngII and nitric oxide during combined heat and hypohydration stress

Cited by 23 publications

References 24 publications

Physiological adaptations of small mammals to desert ecosystems

Physiological adaptations of small mammals to desert ecosystems

Heat Acclimation, Epigenetics, and Cytoprotection Memory

Neuroprotection after Traumatic Brain Injury in Heat-Acclimated Mice Involves Induced Neurogenesis and Activation of Angiotensin Receptor Type 2 Signaling

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