姚泰
自主神经系统对心血管和肾脏活动的调节。
个性化签名
- 姓名:姚泰
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
生理学
- 研究兴趣:自主神经系统对心血管和肾脏活动的调节。
姚泰,男,1938 年生,现任复旦大学上海医学院生理学教授; 1959 年毕业于上海第一医学院医疗系,随即考取同校生理学研究生,于 1962 年毕业。毕业后留校任教。1979 年至 1981 年在瑞典哥德堡大学生理学系福尔柯夫实验室做访问学者。回国后历任上海第一医学院生理学教研室副主任和主任、基础医学部副主任和主任。1986 年晋升生理学教授,并被批准为博士生导师。1988 年被任命为上海医科大学副校长兼研究生院院长。1994 至 2000 年任上海医科大学校长。多年来,姚泰从事生理学教学和科研工作。他的主要研究领域是自主神经系统对心血管和肾脏活动的调节。在西藏工作期间,从事对高海拔地区世居和移居人群生理指标的调查研究。近二十年来,他从事的研究课题包括针刺和刺激躯体神经对心血管和肾脏活动的调整作用、脑内渗透压感受器与交感神经及肾脏活动的关系、血管升压素在心血管活动调节和水盐平衡中的作用、高血压和心肌梗死引起的心肌重构、甾体激素对神经系统的影响等。他的科研成果曾获得国家教委科技进步奖、卫生部医药卫生科技进步奖、中国高校科学技术奖和光华科技基金奖。
1982 年以来,他参加了全国高等医学院校规划教材《生理学》第二、三、四版的编写工作,并担任第五版( 2000 年)、第六版( 2003 年)的主编和七年制临床医学专业规划教材《生理学》( 2001 年)的主编。他还参加了徐丰彦、张镜如主编的大型参考书《人体生理学》第二版的编写工作,并担任第三版( 2001 年)的主编。1997 年,瑞典哥德堡大学授予姚泰荣誉博士学位。目前姚泰担任中国生理学会理事会理事长、《生理学报》编委会主编、医学神经生物学国家重点实验室学术委员会主任等职。
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192
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成果数
5
姚泰, LIAN HU, , DA-NIAN ZHU, ZHANG YU, JOHN Q. WANG, ZHONG-JIE SUN, AND TAI YAO
J Appl Physiol 92: 2153-2161, 2002.,-0001,():
-1年11月30日
Expression of angiotensin II type 1 (AT1) receptor in the rostral ventrolateral medulla in rats. J Appl Physiol 92: 2153–2161, 2002. First published January 11, 2002; 0.1152/japplphysiol.00261.2001.-In the present study, the changes of amino acids release in the spinal cord after the application of angiotensin II (ANG II) in the rostral ventrolateral medulla (RVLM) and the distribution of ANG receptors on neurons of the RVLM were investigated. A microdialysis experiment showed that microinjection of angiotensin II into the RVLM significantly (P<0.01) increased the release of aspartate and glutamate in the intermediolateral column of the spinal cord. Immunofluorescence technique combined with confocal microscopy demonstrated that most of the glutamatergic and GABAergic neurons in the RVLM of both Wistar and spontaneously hypertensive rats (SHR) were double labeled with ANG type 1 (AT1) receptor. Immunocytochemical studies demonstrated that the mean optic density of AT1 receptor of the cell surface as well as the whole cell was higher (P<0.05) in SHR than that in Wistar rats, indicating that the higher expression of AT1 receptors in the RVLM may contribute to the higher responsiveness of SHR to ANG II stimulation. Immunogold staining and electronmicroscopic study demonstrated that AT1 receptor in the RVLM was distributed on the rough endoplasmic reticulum, cell membrane, and nerve processes. The results suggest that effects evoked by ANG II in the RVLM are closely related to glutamatergic and GABAergic pathways. These results indirectly support the hypothesis that ANG II in the RVLM may activate vasomotor sympathetic glutamatergic neurons, leading to an increase in sympathetic nerve activity and arterial blood pressure.
immunofluorescence double staining, glutamatergic, GABAergic, microdialysis, electronmicroscopy
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【期刊论文】Effects of all-trans retinoic acid on angiotensin II-induced myocyte hypertrophy
姚泰, HAO-JIE WANG, YI-CHUN ZHU, AND TAI YAO
J Appl Physiol 92: 2162-2168, 2002.,-0001,():
-1年11月30日
Effects of all-trans retinoic acid on angiotensin II-induced myocyte hypertrophy. J Appl Physiol 92: 2162–2168, 2002. First published January 4, 2002; 10.1152/japplphysiol.01192.2001.-We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate ANG II actions in inducing myocyte hypertrophy. Our observations were as follows. 1) atRA (10-7 to~10-5M) inhibited ANG II-induced hyperplasia of fibroblasts in a dose-dependent manner. 2) Treatment of atRA attenuated the ANG II-induced increase in total cell protein content. 3) Treated with ANG II (10-7M) for 5 days, the cultured neonatal rat cardiac myocytes demonstrated an apparent accumulation of sarcomeric fiber proteins and Golgi's complex, as well as reorganization of the sarcomeric unit within individual myocytes. atRA (10-6M) treatment reduced the accumulation of contractile proteins and Golgi's complex without affecting the ANG II-induced reorganization of the sarcomeric unit. 4) atRA attenuated the ANG II-induced increase in intracellular Ca2+. Our results show that atRA inhibits some effects of ANG II on neonatal rat cardiac myocytes and suggest that atRA may be a therapeutic candidate for the prevention and therapy of cardiac hypertrophy and remodeling.
cardiac hypertrophy, dedifferentiation, intracellular calcium, hyperplasia,, induction of myocyte differentiation
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姚泰, Lei Lu, , Tai Yao, Yi-Zhun Zhu, Guo-Ying Huang, Yin-Xiang Cao, and Yi-Chun Zhu
Am J Physiol Heart Circ Physiol 285: H1370-H1377, 2003.,-0001,():
-1年11月30日
There are in vitro data linking all-trans retinoic acid (atRA) with inhibition of hypertrophy and hyperplasia in cardiomyocytes, vascular smooth muscle cells, and fibroblasts. In the present study, we tested the hypothesis that chronic treatment with atRA may blunt the process of myocardial remodeling in spontaneously hypertensive rats (SHR). Four-week-old male SHR were treated with atRA (5 or 10mg
myocardial hypertrophy, ventricular fibrosis, hypertension
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姚泰, Ying Huanga, Ya-Lin Huangb, Sun Zhanga, Yi-Chun Zhua, Tai Yaoa, b, *
Brain Research 1026(2004)254-260,-0001,():
-1年11月30日
Increasing lines of evidence indicate that estrogen acts as a neuroprotective agent through a nongenomic mechanism. We tested the hypothesis that 17h-estradiol could rapidly attenuate glutamate-induced calcium (Ca2+) overload in rat primary hippocampal neurons via a membrane receptor-dependent mechanism. The bulk cytosolic intracellular Ca2+ level was measured in neurons with fluorescent Ca2+ probe fluo3. Preexposure of primary cultured hippocampal neurons to 17h-estradiol for 3 min attenuated intracellular Ca2+ increase induced by glutamate in a concentration-dependent manner. The action of 17h-estradiol was reversible after washout. Administration of membraneimpermeable 17h-estradiol conjugated to bovine serum albumin (E2–BSA) produced the same effect, suggesting possible involvement of cell membrane receptors. ICI 182,780, a specific estrogen receptor (ER) antagonist, blocked the neuronal response to 17h-estradiol and estradiol BSA, indicating a role of specific ERs. The present study demonstrates that 17h-estradiol acutely reduces glutamate-stimulated intracellular Ca2+ increase via ERs probably on the cell surface of the hippocampal neurons.
Hippocampal neuron, Intracellular calcium, Estradiol, Membrane receptor, Glutamate
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姚泰, Sun ZHANG, Ying HUANG, Yi-chun ZHU, Tai YAO,
Acta Pharmacologica Sinica 2005 Feb; 26 (2): 171-176,-0001,():
-1年11月30日
Aim: To investigate the mechanism of the action of estrogen, which stimulates the release of secreted amyloid precursor protein a (sAPPa) and decreases the generation of amyloid-β protein (Aβ), a dominant component in senile plaques in the brains of Alzheimer's disease patients. Metheds: Experiments were carried out in primary rat cortical neurons, and Western blot was used to detect sAPPa in a culture m edium and the total am ount of cellular amyloid precursor protein (APP) in neurons. Results: 17β-Estradiol (but not 17a-estradiol) andβ-estradiol 6-(0-carboxym ethyl) oxim e: B SA increased the secretion of sAPPa and this effect was blocked by protein kinase C (PKC) inhibitor calphostin C, but not by the classical estrogen receptor antagonist ICI 182, 780. Meanwhile, 17β-estradiol did not alter the synthesis ofcellularAPR Conclusion: The effect of 17β-estradiol unsAPPa secretion is likely mediated through the membrane binding sites, and needs molecular configuration specificity of the ligand. Furthermore, the action of the PKC-dependent pathway might be involved in estrogen-induced sAPPa secretion.
Alzheimer disease, estrogen, amyloid precursor protein, estrogen receptors, protein kinase C
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