The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Yu-wang Miao - One of the best experts on this subject based on the ideXlab platform.
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Blockade of Salusin-β in Hypothalamic Paraventricular Nucleus Attenuates Hypertension and Cardiac Hypertrophy in Salt-induced Hypertensive Rats
Journal of cardiovascular pharmacology, 2015Co-Authors: Da-nian Qin, Yu-ping Suo, Jing Guo, Yu-wang Miao, Wenyan Sun, Wei Cui, Kang ChengAbstract:Abstract:Salusin-β, a multifunctional bioactive peptide, is considered as a promising candidate biomarker for predicting cardiovascular diseases. This study was designed to determine whether inhibition of salusin-β in the Hypothalamic Paraventricular Nucleus (PVN) delays the progression of hypertens
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inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin angiotensin system and proinflammatory cytokines in hypertension
Toxicology and Applied Pharmacology, 2014Co-Authors: Da-nian Qin, Yu-wang Miao, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Zhiming Zhu, Guoqing Zhu, Yuming KangAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
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Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system and proinflammatory cytokines in hypertension
Toxicology and applied pharmacology, 2014Co-Authors: Da-nian Qin, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Yu-wang MiaoAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
Da-nian Qin - One of the best experts on this subject based on the ideXlab platform.
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Blockade of Salusin-β in Hypothalamic Paraventricular Nucleus Attenuates Hypertension and Cardiac Hypertrophy in Salt-induced Hypertensive Rats
Journal of cardiovascular pharmacology, 2015Co-Authors: Da-nian Qin, Yu-ping Suo, Jing Guo, Yu-wang Miao, Wenyan Sun, Wei Cui, Kang ChengAbstract:Abstract:Salusin-β, a multifunctional bioactive peptide, is considered as a promising candidate biomarker for predicting cardiovascular diseases. This study was designed to determine whether inhibition of salusin-β in the Hypothalamic Paraventricular Nucleus (PVN) delays the progression of hypertens
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inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin angiotensin system and proinflammatory cytokines in hypertension
Toxicology and Applied Pharmacology, 2014Co-Authors: Da-nian Qin, Yu-wang Miao, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Zhiming Zhu, Guoqing Zhu, Yuming KangAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
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Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system and proinflammatory cytokines in hypertension
Toxicology and applied pharmacology, 2014Co-Authors: Da-nian Qin, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Yu-wang MiaoAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
Yuming Kang - One of the best experts on this subject based on the ideXlab platform.
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inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin angiotensin system and proinflammatory cytokines in hypertension
Toxicology and Applied Pharmacology, 2014Co-Authors: Da-nian Qin, Yu-wang Miao, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Zhiming Zhu, Guoqing Zhu, Yuming KangAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
Qing Yang - One of the best experts on this subject based on the ideXlab platform.
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inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin angiotensin system and proinflammatory cytokines in hypertension
Toxicology and Applied Pharmacology, 2014Co-Authors: Da-nian Qin, Yu-wang Miao, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Zhiming Zhu, Guoqing Zhu, Yuming KangAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
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Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system and proinflammatory cytokines in hypertension
Toxicology and applied pharmacology, 2014Co-Authors: Da-nian Qin, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Yu-wang MiaoAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
Jun Ren - One of the best experts on this subject based on the ideXlab platform.
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inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin angiotensin system and proinflammatory cytokines in hypertension
Toxicology and Applied Pharmacology, 2014Co-Authors: Da-nian Qin, Yu-wang Miao, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Zhiming Zhu, Guoqing Zhu, Yuming KangAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.
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Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system and proinflammatory cytokines in hypertension
Toxicology and applied pharmacology, 2014Co-Authors: Da-nian Qin, Fu-xin Wang, Jun Ren, Meng Zhang, Qing Yang, Yu-wang MiaoAbstract:Abstract Aims To explore whether reactive oxygen species (ROS) scavenger (tempol) in the Hypothalamic Paraventricular Nucleus (PVN) attenuates renin–angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension. Methods and results Male Sprague–Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 μg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91phox (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1β) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91phox, ACE and IL-1β within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats. Conclusion These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in Hypothalamic Paraventricular Nucleus attenuates the renin–angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension.