Yes! Sex Matters: Sex, the Brain and Blood Pressure

Hay, Meredith; Xue, Baojian; Johnson, Alan Kim

doi:10.1007/s11906-014-0458-4

Cited by 37 publications

(29 citation statements)

References 63 publications

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“…In young male mice, but not cycling young female mice, systemic low-dose AngII-infusion results in a slowly developing increase in blood pressure (Girouard et al 2009, Li et al 2008, Marques-Lopes et al 2015a, Marques-Lopes et al 2014, Marques-Lopes et al 2015b, Pinkerton & Stovall 2010, Tiwari et al 2009, Van Kempen et al 2015b, Xue et al 2013, Xue et al 2005). However, slow-pressor AngII-infusion induces hypertension in OVX mice that model surgical menopause (Hay et al 2014, Xue et al 2013) and in aged rodents (Fortepiani et al 2003, Marques-Lopes et al 2015b, Tiwari et al 2009) that model the acyclicity (Nelson et al 1995) seen in post-menopause. Using a mouse model of Accelerated Ovarian Failure (AOF) that uniquely recapitulates hormonal changes seen in human menopause (Van Kempen et al 2014, Van Kempen et al 2011), we showed that the susceptibility to slow-pressor AngII hypertension begins at emerges at a timepoint that mimics perimenopause (i.e., when estrogens are present but erratically fluctuating) [9].…”

Section: Sex Differences Beyond the Hippocampus: Some Examplesmentioning

confidence: 99%

Understanding the broad influence of sex hormones and sex differences in the brain

McEwen

Milner

2016

J of Neuroscience Research

491

301

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Sex hormones act throughout the entire brain of both males and females via both genomic and non-genomic receptors. Sex hormones can act through many cellular and molecular processes that alter structure and function of neural systems and influence behavior as well as providing neuroprotection. Within neurons, sex hormone receptors are found in nuclei and are also located near membranes where they are associated with presynaptic terminals, mitochondria, spine apparatus, post-synaptic densities. Sex hormone receptors also are found in glial cells. Hormonal regulation of a variety of signaling pathways as well as direct and indirect effects upon gene expression induce spine synapses, up- or down-regulate and alter the distribution of neurotransmitter receptors, regulate neuropeptide expression and cholinergic and GABAergic activity as well as calcium sequestration and oxidative stress. Many neural and behavioral functions are affected, including mood, cognitive function, blood pressure regulation, motor coordination, pain and opioid sensitivity. Subtle sex differences exist for many of these functions that are developmentally programmed by hormones and by not-yet-precisely-defined genetic factors including the mitochondrial genome. These sex differences and responses to sex hormones in brain regions, and upon functions not previously regarded as subject to such differences, indicates that we are entering a new era of our ability to understand and appreciate the diversity of gender-related behaviors and brain functions.

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Section: Sex Differences Beyond the Hippocampus: Some Examplesmentioning

confidence: 99%

Understanding the broad influence of sex hormones and sex differences in the brain

McEwen

Milner

2016

J of Neuroscience Research

491

301

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“…In the brain cortex, ERα mediates neuroprotection during hypoxic/ischemic insults . ERα and ERβ reduce arterial blood pressure through the sympathetic nuclei in the brainstem and hypothalamus . In the model of angiotensin II‐induced hypertension, ERα in the suprafornical organ controls arterial blood pressure .…”

Section: Introductionmentioning

confidence: 99%

Roles of oestradiol receptor alpha and beta against hypertension and brain mitochondrial dysfunction under intermittent hypoxia in female rats

et al. 2019

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Aim Chronic intermittent hypoxia (CIH) induces systemic (hypertension) and central alterations (mitochondrial dysfunction underlying cognitive deficits). We hypothesized that agonists of oestradiol receptors (ER) α and β prevent CIH‐induced hypertension and brain mitochondrial dysfunction. Methods Ovariectomized female rats were implanted with osmotic pumps delivering vehicle (Veh), the ERα agonist propylpyraoletriol (PPT — 30 μg/kg/day) or the ERβ agonist diarylpropionitril (DPN — 100 μg/kg/day). Animals were exposed to CIH (21%‐10% FIO2 — 10 cycles/hour – 8 hours/day – 7 days) or normoxia. Arterial blood pressure was measured after CIH or normoxia exposures. Mitochondrial respiration and H2O2 production were measured in brain cortex with high‐resolution respirometry, as well as activity of complex I and IV of the electron transport chain, citrate synthase, pyruvate, and lactate dehydrogenase (PDH and LDH). Results Propylpyraoletriol but not DPN prevented the rise of arterial pressure induced by CIH. CIH exposures decreased O2 consumption, complex I activity, and increased H2O2 production. CIH had no effect on citrate synthase activity, but decreased PDH activity and increased LDH activity indicating higher anaerobic glycolysis. Propylpyraoletriol and DPN treatments prevented all these alterations. Conclusions We conclude that in OVX female rats, the ERα agonist prevents from CIH‐induced hypertension while both ERα and ERβ agonists prevent the brain mitochondrial dysfunction and metabolic switch induced by CIH. These findings may have implications for menopausal women suffering of sleep apnoea regarding hormonal therapy.

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“…slow-pressor) increase in sympathetic tone and blood pressure [7–12]. However, slow-pressor AngII infusion induces hypertension in ovariectomized mice that model surgical menopause [12, 13] and in aged rodents [8, 10, 14] that model the acyclicity [15] seen in postmenopause. Unfortunately, neither of these approaches has been able to elucidate potential mechanisms related to ovarian hormone irregularity and decline that contribute to perimenopausal hypertension.…”

Section: Introductionmentioning

confidence: 99%

“…In young females, normal estrogen production and estrous cycling may play a key role in attenuating AngII-induced hypertension [12, 13] . Posttranscriptional gene silencing studies have revealed that these protective effects of estrogen on hypertension and ROS production critically involve estrogen receptor (ER) β, but not ERα, in the PVN [33] .…”

Section: Introductionmentioning

confidence: 99%

Redistribution of NMDA Receptors in Estrogen-Receptor-β-Containing Paraventricular Hypothalamic Neurons following Slow-Pressor Angiotensin II Hypertension in Female Mice with Accelerated Ovarian Failure

Marques-Lopes¹,

Tesfaye²,

Israilov³

et al. 2016

Neuroendocrinology

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Hypertension in male and aging female rodents is associated with glutamate-dependent plasticity in the hypothalamus, but existing models have failed to capture distinct transitional menopausal phases that could have a significant impact on the synaptic plasticity and emergent hypertension. In rodents, accelerated ovarian failure (AOF) induced by systemic injection of 4-vinylcyclohexane diepoxide mimics the estrogen fluctuations seen in human menopause including the perimenopause transition (peri-AOF) and postmenopause (post-AOF). Thus, we used the mouse AOF model to determine the impact of slow-pressor angiotensin II (AngII) administration on blood pressure and on the subcellular distribution of obligatory N-methyl-D-aspartate (NMDA) receptor GluN1 subunits in the paraventricular hypothalamic nucleus (PVN), a key estrogen-responsive cardiovascular regulatory area. Estrogen-sensitive neuronal profiles were identified in mice expressing enhanced green fluorescent protein under the promoter for estrogen receptor (ER) β, a major ER in the PVN. Slow-pressor AngII increased arterial blood pressure in mice at peri- and post-AOF time points. In control oil-injected (nonhypertensive) mice, AngII decreased the total number of GluN1 in ERβ-containing PVN dendrites. In contrast, AngII resulted in a reapportionment of GluN1 from the cytoplasm to the plasma membrane of ERβ-containing PVN dendrites in peri-AOF mice. Moreover, in post-AOF mice, AngII increased total GluN1, dendritic size and radical production in ERβ-containing neurons. These results indicate that unique patterns of hypothalamic glutamate receptor plasticity and dendritic structure accompany the elevated blood pressure in peri- and post-AOF time points. Our findings suggest the possibility that distinct neurobiological processes are associated with the increased blood pressure during perimenopausal and postmenopausal periods.

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Yes! Sex Matters: Sex, the Brain and Blood Pressure

Cited by 37 publications

References 63 publications

Understanding the broad influence of sex hormones and sex differences in the brain

Understanding the broad influence of sex hormones and sex differences in the brain

Roles of oestradiol receptor alpha and beta against hypertension and brain mitochondrial dysfunction under intermittent hypoxia in female rats

Redistribution of NMDA Receptors in Estrogen-Receptor-β-Containing Paraventricular Hypothalamic Neurons following Slow-Pressor Angiotensin II Hypertension in Female Mice with Accelerated Ovarian Failure

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