The Experts below are selected from a list of 27 Experts worldwide ranked by ideXlab platform
Justin L. Grobe - One of the best experts on this subject based on the ideXlab platform.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT1A) within the arcuate nucleus (ARC) in the control of energy balance.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT_1A) within the arcuate nucleus (ARC) in the control of energy balance. Recent Findings The development and maintenance of obesity involves suppression of resting metabolic rate (RMR). RMR control is integrated via AgRP and proopiomelanocortin neurons within the ARC. Their projections to other hypothalamic and extrahypothalamic nuclei contribute to RMR control, though relatively little is known about the contributions of individual projections and the neurotransmitters involved. Recent studies highlight a role for AT_1A, localized to AgRP neurons, but the specific function of AT_1A within these cells remains unclear. Summary AT_1A functions within AgRP neurons to control RMR, but additional work is required to clarify its role within subpopulations of AgRP neurons projecting to distinct second-order nuclei, and the molecular mediators of its signaling within these cells.
Lisa L. Morselli - One of the best experts on this subject based on the ideXlab platform.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT1A) within the arcuate nucleus (ARC) in the control of energy balance.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT_1A) within the arcuate nucleus (ARC) in the control of energy balance. Recent Findings The development and maintenance of obesity involves suppression of resting metabolic rate (RMR). RMR control is integrated via AgRP and proopiomelanocortin neurons within the ARC. Their projections to other hypothalamic and extrahypothalamic nuclei contribute to RMR control, though relatively little is known about the contributions of individual projections and the neurotransmitters involved. Recent studies highlight a role for AT_1A, localized to AgRP neurons, but the specific function of AT_1A within these cells remains unclear. Summary AT_1A functions within AgRP neurons to control RMR, but additional work is required to clarify its role within subpopulations of AgRP neurons projecting to distinct second-order nuclei, and the molecular mediators of its signaling within these cells.
Kristin E. Claflin - One of the best experts on this subject based on the ideXlab platform.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT1A) within the arcuate nucleus (ARC) in the control of energy balance.
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Control of Energy Expenditure by AgRP Neurons of the Arcuate Nucleus: Neurocircuitry, Signaling Pathways, and Angiotensin
Current Hypertension Reports, 2018Co-Authors: Lisa L. Morselli, Kristin E. Claflin, Justin L. GrobeAbstract:Purpose of Review Here, we review the current understanding of the functional neuroanatomy of neurons expressing Agouti-related peptide (AgRP) and the Angiotensin 1A Receptor (AT_1A) within the arcuate nucleus (ARC) in the control of energy balance. Recent Findings The development and maintenance of obesity involves suppression of resting metabolic rate (RMR). RMR control is integrated via AgRP and proopiomelanocortin neurons within the ARC. Their projections to other hypothalamic and extrahypothalamic nuclei contribute to RMR control, though relatively little is known about the contributions of individual projections and the neurotransmitters involved. Recent studies highlight a role for AT_1A, localized to AgRP neurons, but the specific function of AT_1A within these cells remains unclear. Summary AT_1A functions within AgRP neurons to control RMR, but additional work is required to clarify its role within subpopulations of AgRP neurons projecting to distinct second-order nuclei, and the molecular mediators of its signaling within these cells.
Dao-wen Wang - One of the best experts on this subject based on the ideXlab platform.
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Effects of RNA interference targeting Angiotensin 1A Receptor on blood pressure and cardiac hypertrophy of rats with renovascular hypertension
Frontiers of Medicine in China, 2008Co-Authors: Jing-qun Zhang, Ye-xin Ma, Dao-wen WangAbstract:The aim of this study is to investigate the effects of RNA interference (RNAi) targeting Angiotensin 1A Receptor (AT1A) on blood pressure and cardiac hypertrophy of rats with renovascular hypertension. Two RNAi plasmids, pAT1A-shRNA1 and pAT1A-shRNA2 each carrying a U6 promoter and an AT1A-specific shRNA-coding template sequence corresponding to the sites 928–946, 978–996 of the mRNA transcript, and a control plasmid pCon carrying a nonspecific shRNA-coding sequence were constructed. Thirty Sprague — Dawley rats with renovascular hypertension (2-kidney 1-clip) were randomly divided into 5 equal groups: Control group (without any intervention), pAT1A-shRNA1, pAT1A-shRNA2, pCon groups (with injection of the corresponding plasmid 4 mg/kg respectively into the tail vein), and valsartan group (30 mg/kg·d−1 by gavage). Three weeks after drug administration, pAT1A-shRNA1, pAT1A-shRNA2 and valsartan respectively resulted in decrease of the tail blood pressure by (15.1 ± 5.4), (16.4 ± 8.4) and (30.6 ± 18.2) mmHg. However, the tail blood pressure increased further by about 25 mmHg in both of pCon and control groups. The carotid artery pressures of pAT1A-shRNA1, pAT1A-shRNA2 and valsartan groups were all significantly lower than those of the control and pCon groups. The ratio of left ventricle weight to body weight (LV/BW) of the rats in pAT1A-shRNA1, pAT1A-shRNA2, and valsartan groups decreased significantly than in the control group (P 0.05). Histopathological examination showed that the myocardiocytes were significantly hypertrophic and the basal membrane of the aorta was significantly thickened in the control group and such changes were alleviated in the pAT1A-shRNA1, pAT1A-shRNA2 and valsartan groups. Compared with the control group, pAT1A-shRNA1 and pAT1A-shRNA2 groups had lowered expression of AT1 Receptor (in the myocardium and the thoracic aorta (all P 0.05). We conclude that RNAi targeting AT1A Receptor inhibits the development of renovascular hypertension and the accompanying cardiac hypertrophy. RNAi technology may become a new strategy of gene therapy for hypertension.
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Effects of RNA interference targeting Angiotensin 1A Receptor on the blood pressure and cardiac hypertrophy of rats with 2K1C hypertension
National Medical Journal of China, 2006Co-Authors: Jing-qun Zhang, Ye-xin Ma, Dao-wen WangAbstract:Objective To investigate the effects of RNA interference (RNAi) targeting Angiotensin 1A (AT1A) Receptor on the blood pressure and cardiac hypertrophy of rats with 2K1C (2-kidney, 1-clip) hypertension. Methods Two kinds of RNAi plasmids, pAT1A-shRNA1 carrying an U6 promoter and an AT1A-specific shRNA-coding template sequence corresponding the sites 928-946 and pAT1A-shRNA2 carrying an U6 promoter and an AT1A-specific shRNA-coding template sequence corresponding the sites 978-996, and a blank plasmid pCon carrying a nonspecific shRNA-coding sequence were constructed. Thirty Sprague-Dawley rats underwent clipping of the left renal artery so as to establish two-kidney, one-clip (2K1C) hypertension models and then were randomly divided into 5 equal groups: pAT1A-shRNA1 group (injected with pAT1A-shRNA1 4 mg/kg only one time), pAT1A-shRNA2 group (injected with pAT1A-shRNA2 4 mg/kg only one time), pCon group (injected with pCon 4 mg/kg only one time), valsartan group (perfused into the stomach with valssartan, a AT1 Receptor inhibitor 30 mg·kg~ -1 ·d~ -1 , for 3 weeks), and control blank group (without any treatment). Three weeks later, the systolic pressure of the caudal artery was measured, catheterization through carotid artery was conducted to measure the systolic blood pressure (SBP) and diastolic blood pressure (DBP), and the left ventricular pressure curve was drawn. Then the rats were killed; the weight of the heart was measured, the ratio of left ventricle weight to body weight (LV/BW) was calculated, and pathological examination of the heart and thoracic aorta was performed. Western blotting was used to detect the protein expression of AT21 in the ventricle and aorta. Six age-matched healthy rats were used as normal controls. Results There was no significant difference in the caudal artery pressure among the 5 groups (all P0.05) before intervention. Three weeks later the caudal artery pressures of the blank control group and pCon group continued to significantly increase by about 25 mm Hg compared to the values before the intervention (both P0.001) and without significant difference between these 2 groups; however, the caudal artery pressures of the pAT1A-shRNA1, pAT1A-shRNA2, and valsartan groups were 15.1 mm Hg±5.4 mm Hg, 16.4 mm Hg±8.4 mm Hg, and 30.6 mm Hg±18.2 mm Hg lower than those before the intervention respectively (all P0.01); and were also significantly lower than those of the blank groups (P0.01 or P0.05).There was no significant differences in the ±dp/dt value and indicators of renal function among these groups. The carotid artery pressure of the pAT1A-shRNA1, pAT1A-shRNA2, and valsartan groups were 194 mm Hg±5 mm Hg, 200 mm Hg±5 mm Hg, and 164 mm Hg±5 mm Hg, all significantly lower than those of the blank and pCon groups (234 mm Hg±10 mm Hg and 232 mm Hg±7 mm Hg respectively, all P0.01). The LV/BW of the pAT1A-shRNA1, pAT1A-shRNA2, and valsartan groups were 2.27±0.37, 2.31±0.26, and 2.26±0.39, all significantly lower than that of the blank and pCon groups (3.24±0.38 and 2.94±0.06, respectively, all P0.01), similar to that of the normal control group (P0.05). The myocardiocytes were significantly hypertrophic and the arterial tunica media was significantly thickened in the blank group and such changes were all improved to different degrees in the pAT1A-shRNA1, pAT1A-shRNA2, and valsartan groups. The protein expression levels of AT1 Receptor in the myocardium of the pAT1A-shRNA and pAT1A-shRNA2 groups were lower by 53.3% and 47.8% respectively than that of the blank group, and the protein expression levels of AT1 Receptor in the thoracic aorta of the pAT1A-shRNA and pAT1A-shRNA2 groups were lower by 58.7% and 49.3% respectively than that of the blank group (all P0.01); however, there were no significant difference in the protein expression levels of AT1 Receptor in the myocardium and thoracic aorta between the valsartan and blank groups (both P0.05). Conclusion RNA interference targeting AT1A Receptor inhibits the development of renovascular hypertension and the accompanying cardiac hypertrophy. The RNAi technology may become a new strategy of gene therapy for hypertension.
Florence Whitehill - One of the best experts on this subject based on the ideXlab platform.
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Angiotensin ii acts through the Angiotensin 1A Receptor to upregulate pendrin
American Journal of Physiology-renal Physiology, 2011Co-Authors: Jill W Verlander, Seongun Hong, Vladimir Pech, James L Bailey, Diana Agazatian, Sharon W Matthews, Thomas M Coffman, Thu H Le, Tadashi Inagami, Florence WhitehillAbstract:Pendrin is an anion exchanger expressed in the apical regions of B and non-A, non-B intercalated cells. Since Angiotensin II increases pendrin-mediated Cl− absorption in vitro, we asked whether ang...
