目的:探讨不同中医治法对高尿酸血症模型大鼠血清AngⅠ,AngⅡ水平的影响。方法:将Wi st ar大鼠135只随机分为空白对照组、模型组、西药治疗组与中药复方(滋肾阴、温肾阳、健脾、活血、化痰及利湿组,每组15只)6个治疗组,除空白对照组外,...目的:探讨不同中医治法对高尿酸血症模型大鼠血清AngⅠ,AngⅡ水平的影响。方法:将Wi st ar大鼠135只随机分为空白对照组、模型组、西药治疗组与中药复方(滋肾阴、温肾阳、健脾、活血、化痰及利湿组,每组15只)6个治疗组,除空白对照组外,其余各组采用腺嘌呤联合乙胺丁醇法建立大鼠高尿酸血症动物模型,造模第21天开始给予各治疗组相应治疗,连续2周。检测血清AngⅠ,AngⅡ水平,观察其变化情况。结果:与模型组比较,除西药治疗组与活血组、利湿组和化痰组血清AngⅠ水平降低外其余治疗组血清AngⅠ水平变化不明显,无显著性差异(P>0.05);西药治疗组与治疗组中的活血组、利湿组和化痰组血清AngⅡ水平明显下降,有显著性差异(P<0.05)。结论:活血、利湿和化痰治法有降低血清AngⅠ水平的趋势;不同中医治法均可降低血清AngⅡ水平,其中以活血、利湿、化痰法治疗效果明显,对高尿酸血症具有治疗作用。展开更多
To explore the relation of angiotensin-converting enzyme （ACE） and angiotensin Ⅱ type 1 receptor （AT1R） gene polymorphism with coronary heart disease （CHD） and the severity of coronary artery stenosis, 130 CHD ...To explore the relation of angiotensin-converting enzyme （ACE） and angiotensin Ⅱ type 1 receptor （AT1R） gene polymorphism with coronary heart disease （CHD） and the severity of coronary artery stenosis, 130 CHD patients who underwent coronary angiography were examined for the number of affected coronary vessels （≥75% stenosis） and coronary Jeopardy score. The insertion/deletion of ACE gene polymorphism and AT1R gene polymorphism （an A→C transversion at nucleotide position 1166） were detected by using polymerase chain reaction （PCR） and restriction fragment length polymorphism （RFLP） in CHD patients and 90 healthy serving as controls. The resuits showed that DD genotype and of ACE were more frequent in CHD patients than that in control group （38.5% vs 14.4%, P〈0.001）. The frequency of the ATIR A/C genotypes did not differ between the patients and the controls （10% vs 13.1%, P〉0.05）. The relative risk associated with the ACE-DD was increased by AT1R-AC genotype. Neither the number of affected coronary vessels nor the coronary score differed among the ACE I/D genotypes （P〉0.05）. But the number of affected coronary vessels and the coronary score were significantly greater in the patients with the AT1R-AC genotype than in those with the AA genotype （P〈0.05）. In conclusion, DD genotype may be risk factor for CHD and MI in Chinese people, and is not responsible for the development of the coronary artery stenosis. The AT1R-C allele may increase the relative risk associated with the ACE-DD genotype, and may be involved in the development of the stenosis of coronary artery.展开更多
Exogenous angiotensin Ⅰ(ANG Ⅰ) was degraded to mainly des-Asp-ANGⅠinstead of ANG Ⅱ in the hypothalarnic homogenate of the Sprague Dawley (SD). Wistar Kyoto (WKY), left renal artery stenosed hypertensive SD (LRAS),...Exogenous angiotensin Ⅰ(ANG Ⅰ) was degraded to mainly des-Asp-ANGⅠinstead of ANG Ⅱ in the hypothalarnic homogenate of the Sprague Dawley (SD). Wistar Kyoto (WKY), left renal artery stenosed hypertensive SD (LRAS), deoxycorticosterone acetale/salt - induced hypertensive SD (DOCA-sall) and spontaneously hypertensive rats (SHR). In the sanie honiogenate, ANG Ⅱ was degraded to ANG Ⅲ, and ANG Ⅲ remained unchanged during 15 min incubation. However, all the homapenates were able to catalyse hippuryl-L-histiayl'-L-leucine to hippuric acid and the catalysis was completely inhibited by 3 PM captorpil. The data showed that angiotensin converting enzyrne presenl in the hypothalamus when extracted by the normal laboratory procedures was not able to hydrolyse ANG Ⅰ to ANG Ⅱ. In addition, the aminopeptidase that degraded ANG Ⅰ to des-Asp-ANG Ⅰ was not inhibited by amastatin, bestatin and EDTA, indicating that it is not aminopeptidase A or B. The formation of hippuric acid was significantly higher in the homapenate of the LRAS whilst the SHR and DOCA-salt showed a significant higher rate of des-Asp-ANG Ⅰ formation. These findings are the first dernonsiration of the formation of des-Asp-ANG Ⅰ as the major product of ANG Ⅰ degradation in the hypothalamic homagenate of the rat. The data also show that in two models of low renin hypertensive rats the formation of nanopeptide is significantly elevated.展开更多
Objective Vascular endothelial cells senescence is one of major risk factors for atherosclerotic diseases,which can be induced by endogenous peptides,such as angiotensin Ⅱ(Ang Ⅱ).However,the effect of chronic Ang Ⅱ...Objective Vascular endothelial cells senescence is one of major risk factors for atherosclerotic diseases,which can be induced by endogenous peptides,such as angiotensin Ⅱ(Ang Ⅱ).However,the effect of chronic Ang Ⅱ stimulation on endothelial senescence remains unknown.Therefore,this study aims to investigate the changes in morphology and function of human umbilical vein endothelial cells(HUVECs)in response to the chronic stimulation of Ang Ⅱ.展开更多
Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect...Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect of angll, captopril on L - Ca maximum current density and sodium maximum current density. Resutls Angll increased the maximum current density compared with control after perfused 5 min, 357. 7 ±219. 7 Vs 279. 5± 240. 5 PA/PF, increase rate is 27. 9 %, the shape of current - voltage relationship curve was unchanged, peaked at + 10 mv, indicated that angll increased L - Ca current density in voltage - dependent. After perfused with captopril, captopril + angll 3, 5 min, L - Ca current was recorded, results suggest L - Ca maximum current density decreased significantly compared with control, in captopril group, 128. 4 ± 92. 6Vs286. 2 ± 89. 7, 66. 7±68. 3Vs 286. 2 ± 89. 7, respectively, rate of inhibition is 55. 1 %, 76. 6 %, respectively. L - Ca current further decreased in captopril perfused 5 min compared with 3 min, 66. 7 ± 68. 3 Vs 128. 4 ± 92. 6, in captopril + angll group, L - Ca current decreased greatly in 3, 5 min than control, 143. 4±117. 6Vs 267. 7±141. 4, 96. 4±82. 5 Vs 267. 7±141. 4, respectively, rate of inhibition is 46. 4 % , 63. 9 % respectively. We also investigated effect of captopril on Na current, which decreased significantly in 1 min and 3 min compared with control, 939. 1 ±319. 1 Vs 1398. 0±144. 6 PA/PF, 469. 95 ± 314. 9 Vs 1398. 0 ±144. 6 PA/PF, respectively, rate of inhibition is 32. 8 % , 66. 3 % , respectively. Na current density decreased significantly in 3 min compared with 1 min, 469. 9±314. 9 Vs 939. 1±319. 1PA/PF, rate of inhibition is 49. 9 % . Conclusions Angiotensin Ⅱexerts increased maximum current density of L - Ca in voltage dependent, captopril decreased maximum current density of L - Ca in voltage dependent, decreased sodium maximum current density, which is the prominently antiarrhythmia mechanisms through inhibition of angiotensin Ⅱ evoked calcium dependent transient inward current and calcium overload.展开更多
文摘目的:探讨不同中医治法对高尿酸血症模型大鼠血清AngⅠ,AngⅡ水平的影响。方法:将Wi st ar大鼠135只随机分为空白对照组、模型组、西药治疗组与中药复方(滋肾阴、温肾阳、健脾、活血、化痰及利湿组,每组15只)6个治疗组,除空白对照组外,其余各组采用腺嘌呤联合乙胺丁醇法建立大鼠高尿酸血症动物模型,造模第21天开始给予各治疗组相应治疗,连续2周。检测血清AngⅠ,AngⅡ水平,观察其变化情况。结果:与模型组比较,除西药治疗组与活血组、利湿组和化痰组血清AngⅠ水平降低外其余治疗组血清AngⅠ水平变化不明显,无显著性差异(P>0.05);西药治疗组与治疗组中的活血组、利湿组和化痰组血清AngⅡ水平明显下降,有显著性差异(P<0.05)。结论:活血、利湿和化痰治法有降低血清AngⅠ水平的趋势;不同中医治法均可降低血清AngⅡ水平,其中以活血、利湿、化痰法治疗效果明显,对高尿酸血症具有治疗作用。
文摘To explore the relation of angiotensin-converting enzyme （ACE） and angiotensin Ⅱ type 1 receptor （AT1R） gene polymorphism with coronary heart disease （CHD） and the severity of coronary artery stenosis, 130 CHD patients who underwent coronary angiography were examined for the number of affected coronary vessels （≥75% stenosis） and coronary Jeopardy score. The insertion/deletion of ACE gene polymorphism and AT1R gene polymorphism （an A→C transversion at nucleotide position 1166） were detected by using polymerase chain reaction （PCR） and restriction fragment length polymorphism （RFLP） in CHD patients and 90 healthy serving as controls. The resuits showed that DD genotype and of ACE were more frequent in CHD patients than that in control group （38.5% vs 14.4%, P〈0.001）. The frequency of the ATIR A/C genotypes did not differ between the patients and the controls （10% vs 13.1%, P〉0.05）. The relative risk associated with the ACE-DD was increased by AT1R-AC genotype. Neither the number of affected coronary vessels nor the coronary score differed among the ACE I/D genotypes （P〉0.05）. But the number of affected coronary vessels and the coronary score were significantly greater in the patients with the AT1R-AC genotype than in those with the AA genotype （P〈0.05）. In conclusion, DD genotype may be risk factor for CHD and MI in Chinese people, and is not responsible for the development of the coronary artery stenosis. The AT1R-C allele may increase the relative risk associated with the ACE-DD genotype, and may be involved in the development of the stenosis of coronary artery.
文摘Exogenous angiotensin Ⅰ(ANG Ⅰ) was degraded to mainly des-Asp-ANGⅠinstead of ANG Ⅱ in the hypothalarnic homogenate of the Sprague Dawley (SD). Wistar Kyoto (WKY), left renal artery stenosed hypertensive SD (LRAS), deoxycorticosterone acetale/salt - induced hypertensive SD (DOCA-sall) and spontaneously hypertensive rats (SHR). In the sanie honiogenate, ANG Ⅱ was degraded to ANG Ⅲ, and ANG Ⅲ remained unchanged during 15 min incubation. However, all the homapenates were able to catalyse hippuryl-L-histiayl'-L-leucine to hippuric acid and the catalysis was completely inhibited by 3 PM captorpil. The data showed that angiotensin converting enzyrne presenl in the hypothalamus when extracted by the normal laboratory procedures was not able to hydrolyse ANG Ⅰ to ANG Ⅱ. In addition, the aminopeptidase that degraded ANG Ⅰ to des-Asp-ANG Ⅰ was not inhibited by amastatin, bestatin and EDTA, indicating that it is not aminopeptidase A or B. The formation of hippuric acid was significantly higher in the homapenate of the LRAS whilst the SHR and DOCA-salt showed a significant higher rate of des-Asp-ANG Ⅰ formation. These findings are the first dernonsiration of the formation of des-Asp-ANG Ⅰ as the major product of ANG Ⅰ degradation in the hypothalamic homagenate of the rat. The data also show that in two models of low renin hypertensive rats the formation of nanopeptide is significantly elevated.
文摘Objective Vascular endothelial cells senescence is one of major risk factors for atherosclerotic diseases,which can be induced by endogenous peptides,such as angiotensin Ⅱ(Ang Ⅱ).However,the effect of chronic Ang Ⅱ stimulation on endothelial senescence remains unknown.Therefore,this study aims to investigate the changes in morphology and function of human umbilical vein endothelial cells(HUVECs)in response to the chronic stimulation of Ang Ⅱ.
文摘Objectives To investigate effect of Angll, captopril on single guinea myocytes on L - type calcium current and sodium current. Methods Membrane patch clamp whole cell recording technique was used to investigate effect of angll, captopril on L - Ca maximum current density and sodium maximum current density. Resutls Angll increased the maximum current density compared with control after perfused 5 min, 357. 7 ±219. 7 Vs 279. 5± 240. 5 PA/PF, increase rate is 27. 9 %, the shape of current - voltage relationship curve was unchanged, peaked at + 10 mv, indicated that angll increased L - Ca current density in voltage - dependent. After perfused with captopril, captopril + angll 3, 5 min, L - Ca current was recorded, results suggest L - Ca maximum current density decreased significantly compared with control, in captopril group, 128. 4 ± 92. 6Vs286. 2 ± 89. 7, 66. 7±68. 3Vs 286. 2 ± 89. 7, respectively, rate of inhibition is 55. 1 %, 76. 6 %, respectively. L - Ca current further decreased in captopril perfused 5 min compared with 3 min, 66. 7 ± 68. 3 Vs 128. 4 ± 92. 6, in captopril + angll group, L - Ca current decreased greatly in 3, 5 min than control, 143. 4±117. 6Vs 267. 7±141. 4, 96. 4±82. 5 Vs 267. 7±141. 4, respectively, rate of inhibition is 46. 4 % , 63. 9 % respectively. We also investigated effect of captopril on Na current, which decreased significantly in 1 min and 3 min compared with control, 939. 1 ±319. 1 Vs 1398. 0±144. 6 PA/PF, 469. 95 ± 314. 9 Vs 1398. 0 ±144. 6 PA/PF, respectively, rate of inhibition is 32. 8 % , 66. 3 % , respectively. Na current density decreased significantly in 3 min compared with 1 min, 469. 9±314. 9 Vs 939. 1±319. 1PA/PF, rate of inhibition is 49. 9 % . Conclusions Angiotensin Ⅱexerts increased maximum current density of L - Ca in voltage dependent, captopril decreased maximum current density of L - Ca in voltage dependent, decreased sodium maximum current density, which is the prominently antiarrhythmia mechanisms through inhibition of angiotensin Ⅱ evoked calcium dependent transient inward current and calcium overload.
