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Role of the central nucleus of the amygdala in regulating the nongenomic effect of aldosterone on sodium intake in rat nucleus tractus solitarius]. PubMed CSCD PKU
期刊论文 | 2018 , 38 (10) , 1159-1164 | Journal of Southern Medical University
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Abstract :

To reveal the nongenomic effect of aldosterone on the regulation of sodium intake in the nucleus tractus solitarius (NTS) and the role of central nucleus of the amygdala (CeA) in regulating this effect.Adult male SD rats were divided into four groups and underwent operations to induce bilateral CeA electrolytic lesions (400 μA, 25 s; <i>n</i>=28), bilateral sham CeA lesions (<i>n</i>=28), unilateral CeA lesions (<i>n</i>=28), or unilateral sham CeA lesions (<i>n</i>=26). After 3 days of recovery, the rats received implantation of a stainless steel 23-gauge cannula wih two tubes into the NTS followed by a recovery period of 7 days. The rats in each group were then divided into two subgroups for microinjection of aldosterone (50 ng/μL) or control solution in the NTS, and the cumulative intake within 30 min of 0.3 mol/L NaCl solution was recorded for each rat.Bilateral CeA lesions (3 days) eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (0.3±0.04 mL in CeA lesion group <i>vs</i> 1.3±0.3 mL in sham lesion group). Unilateral CeA lesion (3 days) reduced aldosterone-induced increase of NaCl intake in the first 15 min (<i>P</i> < 0.05) but not in 15-30 min (<i>P</i> > 0.05). In rats with sham lesions, aldosterone (50 ng/μL) still induced a significant increase in NaCl intake[1.3±0.3 mL <i>vs</i> 0.25±0.02 mL in the control group; F (3, 224)=24.0, <i>P</i> < 0.05].The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake.

Keyword :

nongenomic effect central nucleus of the amygdala sodium intake aldosterone

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GB/T 7714 Qiao Hu , Wang Nan , Yan Jianqun . Role of the central nucleus of the amygdala in regulating the nongenomic effect of aldosterone on sodium intake in rat nucleus tractus solitarius]. [J]. | Journal of Southern Medical University , 2018 , 38 (10) : 1159-1164 .
MLA Qiao Hu 等. "Role of the central nucleus of the amygdala in regulating the nongenomic effect of aldosterone on sodium intake in rat nucleus tractus solitarius]." . | Journal of Southern Medical University 38 . 10 (2018) : 1159-1164 .
APA Qiao Hu , Wang Nan , Yan Jianqun . Role of the central nucleus of the amygdala in regulating the nongenomic effect of aldosterone on sodium intake in rat nucleus tractus solitarius]. . | Journal of Southern Medical University , 2018 , 38 (10) , 1159-1164 .
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Angiotensin II facilitates GABAergic neurotransmission at postsynaptic sites in rat amygdala neurons SCIE PubMed Scopus
期刊论文 | 2018 , 133 , 334-344 | NEUROPHARMACOLOGY
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The central nucleus of the amygdala (CeA) is critical in the regulation of sodium appetite. Angiotensin II (Ang II) is important in the generation of sodium appetite and may function as a neurotransmitter or modulator to affect the synaptic transmission and the excitability of neurons. However, the role of Ang II in the CeA remains unclear. In this study, we determined the effects of Ang II on the excitatory and inhibitory synaptic inputs to the CeA neurons in brain slices with whole-cell patch-clamp recordings. Ang II (0.5-5 mu M) significantly potentiated the amplitude of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) in a concentration-dependent manner. Ang II (2 mu M) significantly increased the amplitude of miniature GABAergic inhibitory postsynaptic currents (mIPSCs) without affecting the frequency. This effect was blocked by Ang II type 1 (AT(1)) receptor antagonist, losartan. One mM guanosine 5'-O-(-2-thiodiphosphate) (GDP-beta-s) in the pipette internal solution eliminated the facilitatory effect of Ang II on GABAergic synaptic transmission. In contrast, Ang II had no effect on the spontaneous glutamatergic excitatory postsynaptic currents (EPSCs) and did not alter the frequency and amplitude of miniature EPSCs at concentrations that facilitated IPSCs. Furthermore, Ang II decreased the firing activity of CeA neurons, and this effect was abolished by losartan and GDP-beta-s. In addition, Ang II failed to inhibit CeA neurons in the presence of bicuculline. These data provide substantial new evidence that Ang II inhibits the CeA neurons by facilitation of GABAergic synaptic input efficacy through activation of postsynaptic ATE receptors. (C) 2018 Elsevier Ltd. All rights reserved.

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GB/T 7714 Hu, Bo , Qiao, Hu , Cao, Tian et al. Angiotensin II facilitates GABAergic neurotransmission at postsynaptic sites in rat amygdala neurons [J]. | NEUROPHARMACOLOGY , 2018 , 133 : 334-344 .
MLA Hu, Bo et al. "Angiotensin II facilitates GABAergic neurotransmission at postsynaptic sites in rat amygdala neurons" . | NEUROPHARMACOLOGY 133 (2018) : 334-344 .
APA Hu, Bo , Qiao, Hu , Cao, Tian , Sun, Bo , Luo, Xiao , Jia, Ru et al. Angiotensin II facilitates GABAergic neurotransmission at postsynaptic sites in rat amygdala neurons . | NEUROPHARMACOLOGY , 2018 , 133 , 334-344 .
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Expression of Proinflammatory Cytokines Is Upregulated in the Hypothalamic Paraventricular Nucleus of Dahl Salt-Sensitive Hypertensive Rats SCIE PubMed Scopus
期刊论文 | 2018 , 9 | FRONTIERS IN PHYSIOLOGY
WoS CC Cited Count: 1 SCOPUS Cited Count: 1
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Accumulating evidence indicates that inflammation is implicated in hypertension. However, the role of brain proinflammatory cytokines (PICs) in salt sensitive hypertension remains to be determined. Thus, the objective of this study was to test the hypothesis that high salt (HS) diet increases PICs expression in the paraventricular nucleus (PVN) and leads to PVN neuronal activation. Eight-week-old male Dahl salt sensitive (Dahl S) rats, and age and sex matched normal Sprague Dawley (SD) rats were divided into two groups and fed with either a HS (4% NaCl) or normal salt (NS, 0.4% NaCl) diet for 5 consecutive weeks. HS diet induced hypertension and significantly increased cerebrospinal fluid (CSF) sodium concentration ([Na+]) in Dahl S rats, but not in normal SD rats. In addition, HS diet intake triggered increases in mRNA levels and immunoreactivities of PVN PICs including TNF-alpha, IL-6, and IL-1 beta, as well as Fra1, a chronic marker of neuronal activation, in Dahl S rats, but not in SD rats. Next, we investigated whether this increase in the expression of PVN PICs and Fra1 was induced by increased CSF [Na+]. Adult male SD rats were intracerebroventricular (ICV) infused with 8 mu l of either hypertonic salt (4 mu mol NaCl), mannitol (8 mu mol, as osmolarity control), or isotonic salt (0.9% NaCl as vehicle control). Three hours following the ICV infusion, rats were euthanized and their PVN PICs expression was measured. The results showed that central administration of hypertonic saline in SD rats significantly increased the expression of PICs including TNF-alpha, IL-6, and IL-1 beta, as well as neuronal activation marker Fra1, compared to isotonic NaCl controls and osmolarity controls. Finally, we tested whether the increase in PICs expression occurred in neurons. Incubation of hypothalamic neurons with 10mM NaCl in a culture medium for 6 h elicited significant increases in TNF-alpha, IL-6, and Fra1 mRNA levels. These observations, coupled with the important role of PICs in modulating neuronal activity and stimulating vasopressin release, suggest that HS intake induces an inflammatory state in the PVN, which, may in turn, augments sympathetic nerve activity and vasopressin secretion, contributing to the development of salt sensitive hypertension.

Keyword :

high salt diet paraventricular nucleus hypertension cerebrospinal fluid proinflammatory cytokines

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GB/T 7714 Jiang, Enshe , Chapp, Andrew D. , Fan, Yuanyuan et al. Expression of Proinflammatory Cytokines Is Upregulated in the Hypothalamic Paraventricular Nucleus of Dahl Salt-Sensitive Hypertensive Rats [J]. | FRONTIERS IN PHYSIOLOGY , 2018 , 9 .
MLA Jiang, Enshe et al. "Expression of Proinflammatory Cytokines Is Upregulated in the Hypothalamic Paraventricular Nucleus of Dahl Salt-Sensitive Hypertensive Rats" . | FRONTIERS IN PHYSIOLOGY 9 (2018) .
APA Jiang, Enshe , Chapp, Andrew D. , Fan, Yuanyuan , Larson, Robert A. , Hahka, Taija , Huber, Michael J. et al. Expression of Proinflammatory Cytokines Is Upregulated in the Hypothalamic Paraventricular Nucleus of Dahl Salt-Sensitive Hypertensive Rats . | FRONTIERS IN PHYSIOLOGY , 2018 , 9 .
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The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats. PubMed Scopus SCIE
期刊论文 | 2018 , 143 , 132-137 | Brain research bulletin
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The central nucleus of the amygdala (CeA) is a critical region in regulating sodium intake, and interestingly, purinergic receptors reportedly related to fluid balance, are also expressed in CeA. In this study, we investigated whether the purinergic mechanisms of CeA were involved in regulating sodium intake. Male Sprague-Dawley rats had cannulas implanted bilaterally into the CeA and were sodium depleted with furosemide (FURO 20 mg/kg) plus 24 h-sodium deficient food fed. Bilateral injections of the P2X purinergic agonist, α,β-methyleneadenosine 5'-triphosphate (α,β-methylene ATP 1.0, 2.0, 4.0 nmol, respectively) into the CeA region induced dose-related reductions in sodium intake without affecting water intake. Injection of P2X purinergic antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS 4.0 nmol/0.5 μl) into the CeA region did not alter sodium and water intake, however, prior injection of PPADS into the CeA area abolished the inhibitory effects on sodium intake by α,β-methylene ATP. Interestingly, prior injection of γ-aminobutyric acid type A (GABAA) receptor antagonist, bicuculline (4.0 nmol/0.5 μl) into the CeA region partially reversed the deficit of sodium intake induced by α,β-methylene ATP. These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABAA receptor.

Keyword :

The central nucleus of the amygdale P2X purinergic receptor Sodium intake GABA

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GB/T 7714 Guan Limin , Qiao Hu , Wang Nan et al. The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats. [J]. | Brain research bulletin , 2018 , 143 : 132-137 .
MLA Guan Limin et al. "The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats." . | Brain research bulletin 143 (2018) : 132-137 .
APA Guan Limin , Qiao Hu , Wang Nan , Luo Xiao , Yan Jianqun . The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats. . | Brain research bulletin , 2018 , 143 , 132-137 .
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Effects of saccharin supplementation on body weight, sweet receptor mRNA expression and appetite signals regulation in post-weanling rats SCIE PubMed Scopus
期刊论文 | 2018 , 107 , 32-38 | PEPTIDES
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Non-nutritive sweeteners have been considered to promote diet healthfulness by delivering a pleasant sweet taste without calories. We investigated the effects of long term supplementation with drinks containing saccharin on body weight and possible mechanisms of the effects in post-weanling rats. Our results showed that saccharin solution intake increased food intake and energy intake in male rats. In males, saccharin solution intake increased TIR3 mRNA expression in the taste buds and ghrelin receptor mRNA expression both in the taste buds and hypothalamus, whereas no effects were observed in females. These results suggest the effects of saccharin solution exposure on food intake and body weight gain may be different in developmental males and females. In males, peripheral sweet taste receptors and both peripheral and central ghrelin receptors may be involved in the effect of saccharin solution intake to promote food intake and weight gain.

Keyword :

Sweet taste receptor Ghrelin Saccharin

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GB/T 7714 Zhao, Xiaolin , Yan, Jianqun , Chen, Ke et al. Effects of saccharin supplementation on body weight, sweet receptor mRNA expression and appetite signals regulation in post-weanling rats [J]. | PEPTIDES , 2018 , 107 : 32-38 .
MLA Zhao, Xiaolin et al. "Effects of saccharin supplementation on body weight, sweet receptor mRNA expression and appetite signals regulation in post-weanling rats" . | PEPTIDES 107 (2018) : 32-38 .
APA Zhao, Xiaolin , Yan, Jianqun , Chen, Ke , Song, Lin , Sun, Bo , Wei, Xiaojing . Effects of saccharin supplementation on body weight, sweet receptor mRNA expression and appetite signals regulation in post-weanling rats . | PEPTIDES , 2018 , 107 , 32-38 .
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TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons SCIE PubMed
期刊论文 | 2017 , 18 (3) , 583-592 | CELL REPORTS | IF: 8.032
WoS CC Cited Count: 18
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The molecular mechanisms underlying acute leptin and serotonin 2C receptor-induced hypophagia remain unclear. Here, we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is sufficient to decrease energy expenditure and increase food intake resulting in elevated body weight. Deficiency of Trpc5 subunits in Pomc neurons is also sufficient to block the anorexigenic effects of leptin and serotonin 2C receptor (Ht2Cr) agonists. The loss of acute anorexigenic effects of these receptors is concomitant with a blunted electrophysiological response to both leptin and Ht2Cr agonists in arcuate Pomc neurons. We also demonstrate that the Ht2Cr agonist lorcaserin-induced improvements in glucose and insulin tolerance are blocked by TrpC5 deficiency in Pomc neurons. Together, our results link TrpC5 subunits in the brain with leptinand serotonin 2C receptor-dependent changes in neuronal activity, as well as energy balance, feeding behavior, and glucose metabolism.

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GB/T 7714 Gao, Yong , Yao, Ting , Deng, Zhuo et al. TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons [J]. | CELL REPORTS , 2017 , 18 (3) : 583-592 .
MLA Gao, Yong et al. "TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons" . | CELL REPORTS 18 . 3 (2017) : 583-592 .
APA Gao, Yong , Yao, Ting , Deng, Zhuo , Sohn, Jong-Woo , Sun, Jia , Huang, Yiru et al. TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons . | CELL REPORTS , 2017 , 18 (3) , 583-592 .
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Ire1 alpha in Pomc Neurons Is Required for Thermogenesis and Glycemia SCIE PubMed
期刊论文 | 2017 , 66 (3) , 663-673 | DIABETES | IF: 7.273
WoS CC Cited Count: 6
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Whether neuronal inositol-requiring enzyme 1 (Ire1) is required for the proper regulation of energy balance and glucose homeostasis is unclear. We found that proopiomelanocortin (Pomc)-specific deficiency of Ire1 alpha accelerated diet-induced obesity concomitant with a decrease in energy expenditure. This hypometabolic phenotype included deficits in thermogenic responses to diet and cold exposure as well as "beiging" of white adipose tissue. We also demonstrate that loss of Ire1 alpha in Pomc neurons impaired whole-body glucose and insulin tolerance as well as hepatic insulin sensitivity. At the cellular level, deletion of Ire1 alpha in Pomc neurons elevated hypothalamic endoplasmic reticulum (ER) stress and predisposed Pomc neurons to leptin and insulin resistance. Together, the current studies extend and confirm conclusions that Ire1 alpha-Xbp1s and associated molecular targets link ER stress in arcuate Pomc neurons to aspects of normal energy and glucose homeostasis.

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GB/T 7714 Yao, Ting , Deng, Zhuo , Gao, Yong et al. Ire1 alpha in Pomc Neurons Is Required for Thermogenesis and Glycemia [J]. | DIABETES , 2017 , 66 (3) : 663-673 .
MLA Yao, Ting et al. "Ire1 alpha in Pomc Neurons Is Required for Thermogenesis and Glycemia" . | DIABETES 66 . 3 (2017) : 663-673 .
APA Yao, Ting , Deng, Zhuo , Gao, Yong , Sun, Jia , Kong, Xingxing , Huang, Yiru et al. Ire1 alpha in Pomc Neurons Is Required for Thermogenesis and Glycemia . | DIABETES , 2017 , 66 (3) , 663-673 .
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Prenatal high-fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat SCIE PubMed Scopus
期刊论文 | 2017 , 25 (5) , 909-919 | OBESITY | IF: 4.042
WoS CC Cited Count: 2 SCOPUS Cited Count: 2
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ObjectiveThis study aimed to determine how the rat placenta and fetus respond to maternal high-fat (HF) diet during gestation and to identify the possible mechanisms. MethodsPregnant Sprague-Dawley rats were fed with standard chow (13.5% fat) or HF (60% fat) diet during gestation. Placentas were collected on gestation day 21. ResultsHF dams had greater fat mass, higher plasma leptin, lower plasma adiponectin, and impaired glucose tolerance during pregnancy. The placental labyrinth thickness was reduced in both male and female fetuses of HF dams. In HF male placentas, glucose transporter 3 gene expression, system A amino acid transporter (SNAT) 2 gene expression, and SNAT2 protein expression were increased through the activation of the mTORC1 4EBP1 branch. In HF female placentas, gene expression of insulin-like growth factor 2 (IGF2) and IGF2 receptor was elevated compared to placentas of females fed standard chow. Although male and female placentas responded differently to prenatal HF diet exposure, both male and female fetal weight was not altered by maternal HF diet. ConclusionsPlacenta responds and adapts to maternal metabolic changes by altering placental layer thickness, mTORC1 signaling, expression of nutrient transporters, and growth factors in a sex-specific manner.

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GB/T 7714 Song, Lin , Sun, Bo , Boersma, Gretha J. et al. Prenatal high-fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat [J]. | OBESITY , 2017 , 25 (5) : 909-919 .
MLA Song, Lin et al. "Prenatal high-fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat" . | OBESITY 25 . 5 (2017) : 909-919 .
APA Song, Lin , Sun, Bo , Boersma, Gretha J. , Cordner, Zachary A. , Yan, Jianqun , Moran, Timothy H. et al. Prenatal high-fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat . | OBESITY , 2017 , 25 (5) , 909-919 .
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Taste sensitivity to sucrose is lower in outbred Sprague-Dawley phenotypic obesity-prone rats than obesity-resistant rats SCIE PubMed Scopus
期刊论文 | 2017 , 489 (2) , 155-163 | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | IF: 2.559
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The purpose of the present study was to better understand the role of sweet taste perception in dietary behavior and body weight in outbred Sprague-Dawley phenotypic obesity-prone and obesity-resistant rats by measuring sucrose taste sensitivity using a conditioned taste aversion paradigm. Rats were given a high fat diet for 2 weeks and were assigned as obesity-prone (P, upper tertile) or obesity-resistant (R, lower tertile) based on weight gain. Each group was then given either chow (C, 10% fat) or the high fat diet (F, 46% fat) for the remainder of the experiment (similar to 18 weeks) such that there were four groups - obesity-prone on chow (C-P), obesity-prone on high fat (H-P), obesity-resistant on chow (C-R), obesity resistant on high fat (H-R). The sucrose sensitivity of phenotypic obesity-prone rats is lower than that of obesity-resistant rats in either H-fed or C-fed group, and all H-fed rats were more sensitivity than their C-fed counterparts (H-P vs. C-P; H-R vs. C-R). Body weight gain and total calories intake of phenotypic obesity-prone rats are more than that of obesity-resistant rats. The results suggest that lower sucrose taste sensitivity may contribute to body weight gain and total calories intake of phenotypic obesity prone rats compared to obesity-resistant rats, and there is correlation between the change in the sweet taste threshold and diet treatment. (C) 2017 Elsevier Inc. All rights reserved.

Keyword :

Sucrose taste sensitivity Conditioned taste aversion Taste detection thresholds Body weight

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GB/T 7714 Sun, Huiling , Yan, Junbao , Sun, Bo et al. Taste sensitivity to sucrose is lower in outbred Sprague-Dawley phenotypic obesity-prone rats than obesity-resistant rats [J]. | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS , 2017 , 489 (2) : 155-163 .
MLA Sun, Huiling et al. "Taste sensitivity to sucrose is lower in outbred Sprague-Dawley phenotypic obesity-prone rats than obesity-resistant rats" . | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 489 . 2 (2017) : 155-163 .
APA Sun, Huiling , Yan, Junbao , Sun, Bo , Song, Lin , Yan, Jianqun . Taste sensitivity to sucrose is lower in outbred Sprague-Dawley phenotypic obesity-prone rats than obesity-resistant rats . | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS , 2017 , 489 (2) , 155-163 .
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Increased activity of the orexin system in the paraventricular nucleus contributes to salt-sensitive hypertension SCIE PubMed Scopus
期刊论文 | 2017 , 313 (6) , H1075-H1086 | AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | IF: 3.569
WoS CC Cited Count: 4 SCOPUS Cited Count: 4
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The orexin system is involved in argininc vasopressin (AVP) regulation, and its overactivation has been implicated in hypertension. However, its role in salt-sensitive hypertension (SSHTN) is unknown. Here, we tested the hypothesis that hyperactivity of the orexin system in the paraventricular nucleus (PVN) contributes to SSHTN via enhancing AVP signaling. Eight-week-old male Dahl salt-sensitive (Dahl S) and age-and sex-matched Sprague-Dawley (SD) rats were placed on a high-salt (HS; 8% NaCl) or normal-salt (NS; 0.4% NaCl) diet for 4 wk. HS intake did not alter mean arterial pressure (MAP), PVN mRNA levels of orexin receptor 1 (OX1R), or OX2R but slightly increased PVN AVP mRNA expression in SD rats. HS diet induced significant increases in MAP and PVN mRNA levels of OX1R, OX2R, and AVP in Dahl S rats. Intracerebroventricular infusion of orexin A (0.2 nmol) dramatically increased AVP mRNA levels and immunoreactivity in the PVN of SD rats. Incubation of cultured hypothalamus neurons from newborn SD rats with orexin A increased AVP mRNA expression, which was attenuated by OX1R blockade. In addition, increased cerebrospinal fluid Na+ concentration through intracerebroventricular infusion of NaCl solution (4 mu mol) increased PVN OX1R and AVP mRNA levels and immunoreactivity in SD rats. Furthermore, bilateral PVN microinjection of the OX1R antagonist SB-408124 resulted in a greater reduction in MAP in HS intake (-16 +/- 5 mmHg) compared with NS-fed (-4 +/- 4 mmHg) anesthetized Dahl S rats. These results suggest that elevated PVN OX1R activation may contribute to SSHTN by enhancing AVP signaling. NEW & NOTEWORTHY To our best knowledge, this study is the first to investigate the involvement of the orexin system in salt-sensitive hypertension. Our results suggest that the orexin system may contribute to the Dahl model of salt-sensitive hypertension by enhancing vasopressin signaling in the hypothalamic paraventricular nucleus.

Keyword :

paraventricular nucleus vasopressin orexin sympathetic nerve activity salt-sensitive hypertension

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GB/T 7714 Huber, Michael J. , Fan, Yuanyuan , Jiang, Enshe et al. Increased activity of the orexin system in the paraventricular nucleus contributes to salt-sensitive hypertension [J]. | AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY , 2017 , 313 (6) : H1075-H1086 .
MLA Huber, Michael J. et al. "Increased activity of the orexin system in the paraventricular nucleus contributes to salt-sensitive hypertension" . | AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 313 . 6 (2017) : H1075-H1086 .
APA Huber, Michael J. , Fan, Yuanyuan , Jiang, Enshe , Zhu, Fengli , Larson, Robert A. , Yan, Jianqun et al. Increased activity of the orexin system in the paraventricular nucleus contributes to salt-sensitive hypertension . | AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY , 2017 , 313 (6) , H1075-H1086 .
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