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Статті в журналах з теми "Angiotensins Physiological effect"
Vatta, M. S., L. G. Bianciotti, A. S. Locatelli, M. L. Papouchado, and B. E. Fernández. "Monophasic and biphasic effects of angiotensin II and III on norepinephrine uptake and release in rat adrenal medulla." Canadian Journal of Physiology and Pharmacology 70, no. 6 (June 1, 1992): 821–25. http://dx.doi.org/10.1139/y92-110.
Повний текст джерелаLin, K. S., J. Y. Chan, and S. H. Chan. "Involvement of AT2 receptors at NRVL in tonic baroreflex suppression by endogenous angiotensins." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 5 (May 1, 1997): H2204—H2210. http://dx.doi.org/10.1152/ajpheart.1997.272.5.h2204.
Повний текст джерелаMezei, Za, Á. Gecse, and G. Telegdy. "The effect of angiotensins on the arachidonate cascade of rat brain microvessels and platelets." International Journal of Psychophysiology 7, no. 2-4 (August 1989): 315–17. http://dx.doi.org/10.1016/0167-8760(89)90253-5.
Повний текст джерелаLancien, Frédéric, Marty Wong, Ali Al Arab, Nagi Mimassi, Yoshio Takei, and Jean-Claude Le Mével. "Central ventilatory and cardiovascular actions of angiotensin peptides in trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 3 (August 1, 2012): R311—R320. http://dx.doi.org/10.1152/ajpregu.00145.2012.
Повний текст джерелаMcGiff, John C., and John Quilley. "20-HETE and the kidney: resolution of old problems and new beginnings." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R607—R623. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r607.
Повний текст джерелаJutte, Sara B., and Jon E. Sprague. "Pharmacologic Regulation of the Renin—Angiotensin System: Physiologic and Pathologic Effects." Journal of Pharmacy Technology 16, no. 4 (July 2000): 138–46. http://dx.doi.org/10.1177/875512250001600408.
Повний текст джерелаTolessa, Debela, Adugna Chala, Kelil Haji, Gizaw Mamo, and Gizaw Eshetu. "Physiological Effects of Angiotensin III." International Journal of Clinical and Experimental Physiology 5, no. 4 (December 30, 2019): 164–67. http://dx.doi.org/10.5530/ijcep.2018.5.4.15.
Повний текст джерелаEvered, Mark D. "Investigating the role of angiotensin II in thirst: Interactions between arterial pressure and the control of drinking." Canadian Journal of Physiology and Pharmacology 70, no. 5 (May 1, 1992): 791–97. http://dx.doi.org/10.1139/y92-105.
Повний текст джерелаFernando, K. C., and G. J. Barritt. "Evidence from studies with hepatocyte suspensions that store-operated Ca2+ inflow requires a pertussis toxin-sensitive trimeric G-protein." Biochemical Journal 303, no. 2 (October 15, 1994): 351–56. http://dx.doi.org/10.1042/bj3030351.
Повний текст джерелаLeal, Marcos André Soares, Thanisia de Almeida, João Guilherme Torres, Luciene Cristina Gastalho Campos, Elisardo Corral Vasquez, and Valério Garrone Barauna. "Physiological and Biochemical Vascular Reactivity Parameters of Angiotensin II and the Action of Biased Agonist TRV023." Advances in Pharmacological and Pharmaceutical Sciences 2020 (March 1, 2020): 1–8. http://dx.doi.org/10.1155/2020/3092721.
Повний текст джерелаДисертації з теми "Angiotensins Physiological effect"
Rajapakse, Niwanthi W. "Paracrine factors and regulation of regional kidney perfusion." Monash University, Dept. of Physiology, 2004. http://arrow.monash.edu.au/hdl/1959.1/9589.
Повний текст джерелаYamada, Yuko. "Studies on an angiotensin AT2 agonist peptide novokinin : physiological effects, mechanisms, and production in genetically modified soybean." Kyoto University, 2008. http://hdl.handle.net/2433/136707.
Повний текст джерела"Characterization of the renin-angiotensin system in silver seabream (sparus sarba): perspectives in salinity adaptation." Thesis, 2005. http://library.cuhk.edu.hk/record=b6074092.
Повний текст джерелаThe renin angiotensin system (RAS) is involved in the control of body fluid homeostasis in silver seabream. Seabream angiotensinogen was cloned and sequenced in the present study. The sequence alignment showed that the angiotensinogen of seabream is most similar to that of pufferfish. Differential status of RAS was found among different salinities, with relatively higher RAS activity among hyperosmotic adapted seabream. Circulating angiotensin II (Ang II) was higher in hyperosmotic adapted seabream, with the highest value observed in seabream adapted to double-strength seawater. Although the level of immunoreactive angiotensins in freshwater adapted seabream was higher than that of brackish-water, Ang III, but not Ang II, was the prevalent circulating form in freshwater adapted seabream according to HPLC analysis. Hepatic angiotensinogen expression, however, did not show any statistical difference among different salinities. A positive feedback control for angiotensinogen by Ang II is present in the hepatic tissue of seabream as Ang II increased the expression of angiotensinogen in isolated hepatocyte but captopril lowered the angiotensinogen expression in intact fish. Branchial Na-K-ATPase activities were elevated by Ang II and the activities among different salinities showed a pattern similar to that of circulating angiotensins. However, upon abrupt hyposmotic transfer, branchial Na-K-ATPase elevated along with a decrease in circulating Ang II, an observation implying that the relationship between Na-K-ATPase and Ang II may only be causal. Captopril blockade not only lowered not only circulating Ang II levels but also that of cortisol, indicating RAS activity may limit cortisol secretion. An elevation in the circulating cortisol may be related to the increase in branchial Na-K-ATPase activities after abrupt hyposmotic transfer. The stimulatory effect on branchial Na-K-ATPase activity and the vasopressor effect of Ang II were more potent in hyposmotic than hyperosmotic adapted seabream, which indicates hyposmotic adapted seabream is more sensitive to RAS activation. The renal RAS in silver seabream functions independently from the systemic RAS as the pattern of renal angiotensins was dissimilar to that of systemic angiotensins. The renal RAS was activated in brackish water conditions and abrupt hyposmotic transfer significantly increased renal RAS activities. Kidney morphometrics also indicated that hyposmotic adaptation increase the filtering capacity of seabream nephrons. The number and diameter of glomeruli increase significantly in freshwater adapted seabream, which may vastly increase the filtering surface of the nephrons. Collecting tubules were more prevalent in the kidney of hyposmotic adapted seabream, with higher number, diameter and thickness, suggesting a lower water permeability of collecting tubules is essential for the formation of copious and diluted urine in hyposmotic environment.
Wong Kwok Shing.
"December 2005."
Adviser: Norman Y. S. Woo.
Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6144.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (p. 130-145).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
"Effect of manipulation of the renin-angiotensin system on the osmoregulatory responses of silver seabream (Sparus sarba) in hyper- and hypo-osmotic media." 2001. http://library.cuhk.edu.hk/record=b5890591.
Повний текст джерелаThesis (M.Phil.)--Chinese University of Hong Kong, 2001.
Includes bibliographical references (leaves 89-107).
Abstracts in English and Chinese.
Title --- p.i
Abstract (English) --- p.ii
Abstract (Chinese) --- p.v
Content --- p.vii
Acknowledgement --- p.x
Abbreviation --- p.xii
Lists of tables and figures --- p.xiii
Chapter Chapter 1 --- General introduction --- p.1
Chapter Chapter 2 --- "Effects of salinity on the cardiovascular responses and dipsogenic behaviors and silver seabream, Sparus sarba."
Chapter 2.1 --- Literature review
Chapter 2.1.1 --- Teleost euryhalinity --- p.5
Chapter 2.1.2 --- Salinity and blood respiratory properties --- p.7
Chapter 2.1.3 --- Salinity and blood volume --- p.8
Chapter 2.1.4 --- Salinity and blood pressure --- p.10
Chapter 2.1.5 --- Intestine physiology --- p.12
Chapter 2.1.6 --- Summary --- p.14
Chapter 2.2 --- Materials and methods
Chapter 2.2.1 --- Experimental animals --- p.19
Chapter 2.2.2 --- Salinity adaptation --- p.19
Chapter 2.2.3 --- Drinking rate measurement --- p.19
Chapter 2.2.4 --- Respiratory characteristics --- p.20
Chapter 2.2.5 --- Blood volume measurement --- p.21
Chapter 2.2.6 --- Blood pressure experiment --- p.23
Chapter 2.2.7 --- Statistical analysis --- p.23
Chapter 2.3 --- Results
Chapter 2.3.1 --- Drinking rate --- p.25
Chapter 2.3.2 --- Oxygen dissociation curves --- p.27
Chapter 2.3.3 --- Blood volume --- p.29
Chapter 2.3.4 --- Blood pressure --- p.31
Chapter 2.4 --- Discussion
Chapter 2.4.1 --- Drinking rate --- p.36
Chapter 2.4.2 --- Oxygen dissociation curves --- p.37
Chapter 2.4.3 --- Blood volume --- p.38
Chapter 2.4.4 --- Blood pressure --- p.40
Chapter Chapter 3 --- "Manipulation of renin-angiotensin system in relation to the cardiovascular responses and dipsogenic behaviors of silver seabream, Sparus sarba."
Chapter 3.1 --- Literature review
Chapter 3.1.1 --- Renin angiotensin system (RAS) --- p.41
Chapter 3.1.2 --- RAS and blood pressure --- p.47
Chapter 3.1.3 --- RAS and drinking --- p.53
Chapter 3.1.4 --- RAS and Cortisol --- p.55
Chapter 3.1.5 --- RAS and kidney --- p.58
Chapter 3.1.6 --- Summary --- p.58
Chapter 3.2 --- Materials and methods
Chapter 3.2.1 --- Experimental animals --- p.61
Chapter 3.2.2 --- Salinity adaptation --- p.61
Chapter 3.2.3 --- Drinking rate measurement --- p.61
Chapter 3.2.4 --- Determination of angiotensin converting enzyme (ACE) activity --- p.61
Chapter 3.2.5 --- Blood pressure experiment --- p.62
Chapter 3.2.6 --- Statistical analysis --- p.63
Chapter 3.3 --- Results
Chapter 3.3.1 --- Drinking rate --- p.64
Chapter 3.3.2 --- ACE activity --- p.69
Chapter 3.3.3 --- Blood pressure --- p.71
Chapter 3.4 --- Discussion
Chapter 3.4.1 --- Drinking rate --- p.77
Chapter 3.4.2 --- ACE activity --- p.81
Chapter 3.4.3 --- Blood pressure --- p.83
Chapter Chapter 4 --- General conclusion --- p.86
Reference --- p.89
"Potential roles of angiotensin ii, glucagon like peptide-1 and vitamin D systems in pancreatic islet function." 2010. http://library.cuhk.edu.hk/record=b5549581.
Повний текст джерела在第一部分的研究裡,我們檢測了阻斷血管緊張素一型受體(纈沙坦)和增強GLP-l 作用(DPPIV 抑制劑LAF237) 的復合效應對二型糖尿病小鼠(db/db) 血糖控制和胰島功能方面的影響。我們比較了接受單一給藥和聯合給藥的db/db 小鼠的胰島功能。所有的藥物處理都改善了db/db 小鼠的血糖穩態,而聯合給藥組在增加胰島B細胞面積,減少細胞凋亡,促進增殖以及降低膜島氧化應激和膜島纖維化方面體現出復合效應。另外,短期的聯合給藥顯著促進分離出來的胰島細胞的胰島素分泌。這些結果顯示了血管緊張素型受體阻斷劑和DPPIV 抑制劑在改善胰島的結構與功能以及治療二型糖尿病方面具有復合效應。
據研究,維生素D 是種具有抗糖尿病和高血壓作用的荷爾蒙,而不適合的RAS活性能夠減少胰島功能和糖耐量。維生素D 對腎臟腎素的直接抑制作用表明維生素D 可能可以調節胰島得局部RAS 活性進而調節胰島的生理作用。因此第二部分的實驗旨在研究維生素D 是否能夠抑制分離培養的胰島中非正常表達的胰島局部RAS組分並且改善胰島且細胞功能。維生素D 受體存在於胰島且細胞的核與質中,計量依賴性地調節受體對活性維他命D-骨化三醇的反應。骨化三醇的刺激可以通過增加維生素D24羥化黣激發胰島局部維他命D 系統的反饋機制。在分離的胰島中,長期處於高糖的環境,胰島局部RAS 的異常表達可以一定濃度的骨化三醇治療和預防。然而,骨化三醇的送科治療效果,並沒有在生理正常糖濃度的情況下被發現。另外,在高糖環境下,骨化三醇增加胰島素前體合成以及葡萄糖刺激的服島素分泌。這些結果顯示骨化三醇能夠調節以及保護高糖環境引起的異常胰島RAS 組分表達並通過增加胰島素的合成與分泌來改善胰島的功能,為在高血糖和糖尿病情況下的維生素D 與胰島功能關系提供了新的機制。
循環中的維生素D 水平與血糖濃度以及糖尿病的患病風險成反比。第二部分的實驗結果現實了維生素D 具有潛在的調節胰島RAS 進而調節胰島功能的作用。因此,在第三部分的實驗裡,我們假設不充足的維生素D 水平可能引起異常的胰島RAS 表達進而引起胰島功能障薇。為了這個目的,我們使用了維生素D 受體缺失的基因敲除小鼠和維生素D 缺乏小鼠來檢測糖代謝,膜島形態以及局部RAS 組分的表達。結果顯示,在缺乏維生素D 以及正常的維生素D 作用的情況下,胰島局部RAS 組分異常表達。而這個維生素D 導致的RAS 異常表達的作用可能發生在高血糖現象之前,從而導致了胰島功能障礙,異常的糖代謝以及減弱的胰島且細胞本身的胰島素作用。這些結果為在生理情況下,維生素D 可以通過調節胰島局部RAS 的表達進而調節胰島功能提供了有力的支持。
總括來說,胰島局部RAS 在持續高糖環境下的胰島功能中有著關鍵的作用。GLP-l 和維生素D 都與胰島RAS 具有潛在的生物相關性並可以影響RAS 的表達,進而調節胰島功能和自細胞體積。我們的實驗數據顯示了這三種調節系統共同作用並調節目突島細胞功能以及血糖穩態,進一步提議了它們在二型糖尿病治療中的價值。
Pancreatic islets perfonn critical biological activities by means of synthesizing and releasing islet peptide honnones, notably insulin that controls our glucose homeostasis. The insulin secretory function is, in turn, governed by various conditions and signaling molecules. In the past decade, it is recognized that the renin-angiotensin system (RAS) has local function rather than the maintenance of blood pressure and fluid homeostasis. With our recent recognition of an islet RAS, it is believed that it has novel roles in islet physiology and diabetes. Meanwhile, more and more clinically relevant regulators that have pivotal roles in islet function and diabetes have been well investigated; such regulators have positive action on insulin secretion, B-cell replication and cell apoptosis/proliferation balance. Of great interest in this context is the glucagon-like peptide I (GLP-I) that improves islet function and glycemic control via its islet specific receptors located on the islets. On the other hand,vitamin D also regulates islet insulin secretion and diabetes via its mediation of receptors on islet B-cells. Like islet RAS, GLPI and vitamin D exert their biological effects via mediation of respective receptors located on the common target, i.e. the islet beta-cells. As such, it is plausible to propose that all these three regulators have potential interactions so as to affect islet functions in a direct or an indirect manner. Accordingly, the primary objective of this study is to examine the potential roles oflocal RAS, GLP-I and vitamin D system in pancreatic islet function. The present study is thus divided into three main parts addressing the issues of these three novel regulators in islet function: (1) the potential synergism of GLP-I and RAS in islet function; (2) the modulatory effects of vitamin D on islet RAS expression and function; (3) The altered islet RAS and islet function under a hypovitaminosis D condition.
In the first part of our study, we examined the combined effect of blocking islet A Tl receptor (ATl receptor blocker: valsartan) and enhancing GLP-l actions (DPP IV inhibitor: LAF237) on islet function and glycemic control in a mouse model with type 2 diabetes, db/db mice. We compared the islet function in db/db mice with either valsartan or LAF237 mono treatment or combined treatment. Consistently, all these treatments improved glucose homeostasis in db/db mice while combined treatment resulted in a significant increase in islet B-cell area by decreasing cell apoptosis and increasing proliferation, together with marked decreases of islet oxidative stress and fibrosis. In addition, a short-term effect on stimulating insulin secretion was also observed in isolated islets with combined treatment. These results indicate that the combination treatments with ATl receptor blocker and DPP IV inhibitor has beneficial additive effects on islet structure and function in type 2 diabetes, compared with their monotherapeutic treatments.
It is reported that vitamin D is a hormone with anti-diabetic and anti-hypertension effects in human while inappropriate RAS activity has been known to reduce islet function and glucose tolerance. The direct suppressive effect of vitamin D on renal renin activity indicates vitamin D may acts as a regulator in RAS activity thus modulate islet physiology. In the second part of our study, it was aimed to study whether vitamin D vitamin D downregulation of abnormal islet RAS activity improves B-cell function using an isolated pancreatic islet model. VDR was localized in islet B-cell nuclei and cytoplasm, mediated responses to active form of vitamin D calcitriol in a dose-dependent manner. This islet local vitamin D system may have its own feedback system as a marked increase ofCYP24 transcription was triggered by calcitriol stimulation. In isolated islets exposed to prolonged high glucose environment, abnormal expressed islet RAS components could be reversed or protected by calcitriol at a specific concentration. However, the inhibition effect of calcitriol on islet RAS were not observed at physiological glucose concentrations. In additon, calcitriol increased islet proinsulin synthesis and insulin secretion with hyperglycemia. These results indicated that calcitriol modulate or protect the abnormal isolated islet RAS component expression against hyperglycemia and improve islet function via increasing insulin synthesis and secretion, which might provide an alternative mechanism by which vitamin D availability enhances islet function in hyperglycemia or diabetes.
The circulating vitamin D level is inversely related to blood glucose level and risks of diabetes. Results in the second part of experiments suggested the potential RAS modulatory effect of vitamin D in isolated islets Therefore, in the third part of our study, we hypothesize that the insufficient vitamin D levels may lead to the inappropriate regulation of islet RAS expression and thus result in islet dysfunction. To achieve this, we examined the potential islet RAS-mediated effect of vitamin D on islet function by accessmg glucose homeostasis, islet histomorphology, and local RAS expression and function by means of using a vitamin D receptor knockout and diet-induced vitamin D deficiency mouse models. Results showed that the islet RAS components were abnormally expressed when lacking a sufficient vitamin D level and normal vitamin D action. These observed effects of insufficient vitamin D might occur prior to onset of hyperglycemia thus modulating islet RAS expression, which in turn lead to islet failure and dysfunctional glucose homeostasis, together with decreased insulin actions in islet B-cells. These results provide supports for the view that vitamin D physiologically exerts modulatory effects on islet function by downregulating islet RAS expression and function.
In summary, islet local RAS may have a central role in islet function under prolonged hyperglycemic stress. GLP-l and vitamin D have biological interactions with the islet RAS by downregulation of its expression and function, thereby affecting islet cell function and cell mass. Our data indicate that all three regulators work together in the regulation of pancreatic islet B-cell functions and glucose homeostasis, further suggestive of their potential values in the treatment of type 2 diabetes.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Cheng, Qianni.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2010.
Includes bibliographical references (leaves [205]-243).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Abstract --- p.i
摘要 --- p.v
Acknowledgements --- p.viii
List of Publications --- p.x
Table of Contents --- p.xii
List of Abbreviations --- p.xvi
Chapter Chapter 1 --- General Introduction --- p.1
Chapter 1.1 --- Endocrine Pancreas --- p.2
Chapter 1.1.1 --- The structure and composition of endocrine pancreas --- p.3
Chapter 1.1.2 --- Functions of endocrine pancreas --- p.4
Chapter 1.1.3 --- Insulin structure and insulin receptors --- p.8
Chapter 1.1.4 --- Mechanisms of insulin secretion --- p.11
Chapter 1.1.5 --- Mechanisms of insulin actions --- p.18
Chapter 1.1.6 --- Disorders of the endocrine pancreas --- p.22
Chapter 1.2 --- Diabetes mellitus --- p.23
Chapter 1.2.1 --- Type 1 diabetes mellitus (TlDM) --- p.24
Chapter 1.2.2 --- Type 2 diabetes mellitus (T2DM) --- p.26
Chapter 1.2.3 --- Other types of diabetes mellitus --- p.29
Chapter 1.2.4 --- Islet dysfunction and T2DM --- p.30
Chapter 1.3 --- Renin-angiotensin system (RAS) --- p.33
Chapter 1.3.1 --- Components ofRAS --- p.33
Chapter 1.3.2 --- Tissue local RAS --- p.42
Chapter 1.3.3 --- Pancreatic local RAS --- p.43
Chapter 1.4 --- Glucagon like peptide-l (GLP-l) and pancreatic islet function --- p.54
Chapter 1.4.1 --- Gastrointestinal incretin honnones --- p.54
Chapter 1.4.2 --- GLP-l and pancreatic islet function --- p.56
Chapter 1.4.3 --- Incretin based therapies for T2DM --- p.59
Chapter 1.4.4 --- GLP-lIRAS axis and pancreatic islet function --- p.62
Chapter 1.5 --- Vitamin D and pancreatic islet function --- p.64
Chapter 1.5.1 --- Vitamin D synthesis and metabolism --- p.65
Chapter 1.5.2 --- Vitamin D physiological functions and pancreatic islets --- p.67
Chapter 1.5.3 --- Vitamin D and diabetes mellitus --- p.68
Chapter 1.5.4 --- Vitamin D and RAS --- p.70
Chapter 1.6 --- Objectives --- p.71
Chapter Chapter 2 --- Materials and Methods --- p.73
Chapter 2.1 --- Experimental animal models --- p.74
Chapter 2.1.1 --- Animal model ofT2DM --- p.74
Chapter 2.1.2 --- Animal model for pancreatic islet isolation --- p.75
Chapter 2.1.3 --- Vitamin D receptor knockout mice (VDRKO mice) --- p.75
Chapter 2.1.4 --- Animal model for vitamin D deficiency --- p.76
Chapter 2.2 --- Pancreatic islet isolation and culture --- p.76
Chapter 2.2.1 --- Mice pancreatic islet and single B-cell isolation --- p.77
Chapter 2.2.2 --- Primary culture of isolated pancreatic islets: --- p.78
Chapter 2.3 --- Physiological assay for pancreatic islet function --- p.78
Chapter 2.3.1 --- Measurement of blood glucose and glucose tolerance test --- p.78
Chapter 2.3.2 --- Measurement of glucose-induced insulin secretion --- p.79
Chapter 2.3.3 --- Measurement of (pro )insulin biosynthesis --- p.80
Chapter 2.4 --- Detection ofmRNA expression --- p.80
Chapter 2.4.1 --- Design of primers --- p.81
Chapter 2.4.2 --- mRNA extraction and cDNA synthesis --- p.82
Chapter 2.4.3 --- Detection of mRN A expression by conventional peR --- p.83
Chapter 2.4.4 --- SYBR Green real-time peR --- p.83
Chapter 2.4.5 --- Real-time peR analysis using the comparative eT method --- p.84
Chapter 2.5 --- Detection of protein expression --- p.84
Chapter 2.5.1 --- Western blot analysis --- p.84
Chapter 2.5.2 --- Immunostaining assessment --- p.85
Chapter 2.6 --- In situ detection of oxidative stress, proliferation and apoptosis --- p.88
Chapter 2.6.1 --- Detection of islet reactive oxygen species --- p.88
Chapter 2.6.2 --- Detection of cell proliferation --- p.89
Chapter 2.6.3 --- Measurement of cell apoptosis --- p.90
Chapter 2.7 --- Statistical data analysis --- p.90
Chapter Chapter 3 --- Combination of DPP-IV Inhibitor LAF237 with ATl Receptor Antagonist Valsartan Enhances Pancreatic Islet Morphology and Function in a Mouse Model of Type 2 Diabetes (This work has been published in J Pharmacal Exp Ther, 327: PI-9) --- p.91
Chapter 3.1 --- Abstract --- p.92
Chapter 3.2 --- Introduction --- p.94
Chapter 3.3 --- Materials and Methods --- p.96
Chapter 3.4 --- Results --- p.103
Chapter 3.4.1 --- Effects of acute treatment with GLP-I and valsartan on insulin secretion in isolated islets --- p.103
Chapter 3.4.2 --- Effects of LAF237 and valsartan on pancreatic --- p.105
Chapter 3.4.3 --- Effects of LAF237 and valsartan on --- p.107
Chapter 3.4.4 --- Effects ofLAF237 and valsartan on islet apoptosis --- p.109
Chapter 3.4.5 --- Effects of LAF237 and valsartan on islet fibrosis --- p.110
Chapter 3.4.6 --- Effects of LAF237 and valsartan on pancreatic islet superoxide and nitrotyrosine expression --- p.113
Chapter 3.4.7 --- Effects of LAF237 and valsartan on bood glucose concentration and glucose tolerance in db/db diabetic mice --- p.116
Chapter 3.5 --- Discussion --- p.119
Chapter Chapter 4 --- The Role of Calcitriol in Modulating the Expression and Function of Islet Renin-Angiotensin System in Isolated Mouse Pancreatic Islets --- p.124
Chapter 4.1 --- Abstract --- p.125
Chapter 4.2 --- Introduction --- p.127
Chapter 4.3 --- Materials and Methods --- p.130
Chapter 4.4 --- Results --- p.135
Chapter 4.4.1 --- The expression of islet VDR under different glucose conditions and the effects of calcitriol --- p.135
Chapter 4.4.2 --- The effect of calcitriol on high glucose-modulated islet RAS component expression --- p.140
Chapter 4.4.3 --- The protective effect of calcitriol against high glucose on islet RAS component expression --- p.144
Chapter 4.4.4 --- The effect of calcitriol on (pro )insulin biosynthesis and insulin release in isolated islets --- p.148
Chapter 4.5 --- Discussion --- p.151
Chapter Chapter 5 --- Altered Islet Local Renin-Angiotensin System and Islet Function in Mice with Hypovitaminosis D --- p.158
Chapter 5.1 --- Abstract --- p.159
Chapter 5.2 --- Introduction --- p.160
Chapter 5.3 --- Materials and methods --- p.163
Chapter 5.4 --- Results --- p.168
Chapter 5.4.1 --- Glucose homeostasis and islet morphology in VDR KO mice --- p.168
Chapter 5.4.2 --- Expression of vitamin D receptor and major RAS components in the pancreatic islets of WT and VDR KO mice --- p.170
Chapter 5.4.3 --- Vitamin D deficiency in mice on a vitamin D deficient diet --- p.172
Chapter 5.4.4 --- Altered glucose homeostasis in vitamin D deficient mice --- p.174
Chapter 5.4.5 --- Islet histomorphology in vitamin D deficient mice --- p.176
Chapter 5.4.6 --- Regulation of islet RAS components expression in vitamin D deficient mice --- p.179
Chapter 5.4.7 --- Transcriptional regulation of islet insulin receptor and its substrates in vitamin D deficient mice --- p.181
Chapter 5.4.8 --- Effect of calcitriol treatment on glucose tolerance in vitamin D deficient mice --- p.183
Chapter 5.5 --- Discussion --- p.185
Chapter Chapter 6 --- General Discussion --- p.191
Chapter 6.1 --- Combination effects of blocking islet RAS components and enhancing incretin activity on improving islet function in type 2 diabetes --- p.193
Chapter 6.2 --- Potential modulatory effect of vitamin D on islet RAS expression and action --- p.196
Chapter 6.3 --- The role of vitamin D in modulating islet RAS in glucose homeostasis and islet function --- p.199
Chapter 6.4 --- The significance ofRAS, GLP-l and vitamin D in the management of T2DM --- p.201
Chapter 6.5 --- Conclusion --- p.202
Chapter 6.6 --- Future studies --- p.202
Chapter Chapter 7 --- Bibliography --- p.205
"Endothelial cyclooxygenase-2 mediates endothelium-dependent contractions and angiotensin II-induced vascular inflammation." Thesis, 2010. http://library.cuhk.edu.hk/record=b6075038.
Повний текст джерелаIn the first part of the study, I investigated whether COX-2 participated in the occurrence of endothelium-dependent contractions in the aortae from young (-3 month-old) hamsters and identified the most possible EDCF. Endothelium-dependent contractions were elicited by acetylcholine and abolished by COX-2 inhibitors (NS-398, DuP-697 and celecoxib) and thromboxane-prostanoid (TP) receptor antagonists (S 18886, L-655,240 and GR 32191), but not by COX-1 inhibitors (valeryl salicylate and sc 560). RT-PCR and Western blot analysis using aortae with and without endothelium revealed that the COX-2 expression was localized mainly in the endothelium. Levels of prostangladin F2alpha (PGF2alpha ) and prostacyclin (PGI2) increased in response to acetylcholine and the release of both prostaglandins was inhibited by COX-2 but not COX-1 inhibitors. Exogenous PGF2alpha but not PGI2 caused contractions at a concentration that corresponded to the amount released endogenously. The release of PGF2alpha was not affected by the presence of nitric oxide (NO). The results of the present study suggest that a novel constitutive role of COX-2 in endothelium-dependent contractions, with its metabolites PGF2alpha acting as a physiological EDCF in the young hamster aortae.
In the third part of the study, I investigated the relationship and the intracellular signaling cascades linking two pro-inflammatory factors Ang II and COX-2, and tested whether COX-2 mediated the Ang II-induced vascular pathogenesis. Eight hour-incubation with 100 nmol/L Ang II resulted in maximal COX-2 expression in primary rat endothelial cells and it was inhibited by losartan and RNA synthesis inhibitor (actinomycin-D). Inhibitors of either p38 MAPK or ERK1/2 (respectively SB 202190 and PD 98059) decreased the COX-2 expression, and co-treatment with both inhibitors caused an additive effect, suggesting a joint mediation through both kinases. Protein kinase C (PKC) inhibitor (GF109203X), and particularly, the specific PKCdelta inhibitor (rottlerin), prevented Ang II-induced phosphorylation of ERK1/2 and COX-2 expression, indicating an upstream regulation of ERK1/2 by PKC delta. A pivotal role of PKCdelta in Ang II-induced COX-2 expression was further supported by a similar stimulatory effect of PKC activator, signified by the Ang II-stimulated translocation of PKCdelta to the membrane and confirmed by its phosphorylation (Tyr311). Small interfering RNA targeting PKCdelta (siPKCdelta) diminished COX-2 expression, which was abrogated in siPKCdelta-treated cells treated with SB 202190, confirming the parallel pathways of PKC delta-ERK1/2 and p38 MAPK. Aortae and renal arteries from Ang II-infused rats exhibited an increased endothelial COX-2 expression and impaired acetylcholine-induced relaxation that was normalized by celecoxib. Human mesenteric arteries incubated with Ang II demonstrated elevated endothelial COX-2 and MCP-1 expressions, of which the former was inhibited by SB 202190 plus rottlerin and the latter prevented by COX-2 inhibitor celecoxib. Renal arteries from hypertensive or diabetic patients revealed an exaggerated expression of COX-2 and MCP-1 in the endothelium. The present novel findings indicate that the activation of PKCdelta-ERK1/2 and p38 MAPK is critical in Ang II-induced COX-2 up-regulation in endothelial cells, and identify a COX-2-dependent pro-atherosclerotic cytokine MCP-1. (Abstract shortened by UMI.)
Wong, Siu Ling.
Adviser: Huang Yu.
Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2010.
Includes bibliographical references (leaves 192-228).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
"A central role of the renin-angiotensin system in estrogen deficiency-related endothelial dysfunction and its prevention." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074574.
Повний текст джерелаFunctional studies showed that acetylcholine-induced relaxations in isolated aortas were impaired in a time-dependent manner, from the 4th-week to the 12th-week after ovariectomy. The impaired relaxations were partially restored by acute treatment with losartan [angiotensin II type 1 receptor (AT1R) blocker] and apocynin [NAD(P)H oxidase inhibitor]. The present results demonstrate that estrogen deficiency blunted endothelium-dependent relaxations due to impaired the NO bioavailability, which is closely associated with the reduced eNOS activity and elevated RAS expression and associated NAD(P)H oxidase-mediated oxidative stress in the vascular wall.
The present study shows that chronic consumption of cranberry juice restored the endothelium-dependent relaxations in aortas from ovariectomized rats. In ovariectomized rats, the phenylephrine-induced a higher active vascular tension; which was prevented by chronic consumption of cranberry juice. The present data also shows that cranberry juice administration significantly reduces the elevated serum levels of total cholesterol, triglyceride, high density lipoprotein (HDL) cholesterol, non-HDL (nHDL) cholesterol, and nHDL/HDL. The active ingredients in the cranberry juice organic extract accounting for the vascular benefit remain to be further examined even though the extract causes endothelial NO-dependent relaxations in normal rat aortas and contains several bioactive compounds, some of which may protect the vascular function. This study provides the first line of evidence concerning a significant vascular benefit of chronic consumption of cranberry juice during estrogen deficiency. (Abstract shortened by UMI.)
The present study used ovariectomized female rats that mimic the "equivalent" state of menopause in human and investigated whether dysregulation of RAS components contribute to endothelial dysfunction and whether chronic treatment with ACEI (enalapril) or ARB (valsartan) could restore endothelial function in ovariectomized rats.
The second objective of the present study was to investigate whether or not consumption of cranberry juice, a popular drink in Western countries, could restore endothelial function during estrogen deficiency and to elucidate the cellular mechanisms underlying the improved endothelial function.
Yung, Lai Ming.
Adviser: Huana Yu.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3252.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 148-168).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
Книги з теми "Angiotensins Physiological effect"
Timmermans, P. B. M. W. M. and Wexler Ruth R, eds. Medicinal chemistry of the renin-angiotensin system. Lausanne: Elsevier, 1994.
Знайти повний текст джерелаInternational Symposium on Cellular and Molecular Biology of the Adrenal Cortex (5th 1992 Avignon, France). Cellular and molelcular biology of the adrenal cortex: Proceedings of the 5th International Symposium on Cellular and Molecular Biology of the Adrenal Cortex held in Avignon (France) August 27-29, 1992. Paris, France: INSERM, 1992.
Знайти повний текст джерелаDing, Lili. The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats. St. Catharines, Ont: Brock University, Faculty of Applied Health Science, 2005.
Знайти повний текст джерелаAhsan, Husain, Graham Robert M, and Victor Chang Cardiac Research Institute., eds. Drugs, enzymes, and receptors of the renin-angiotensin system: Celebrating a century of discovery. Amsterdam: Harwood Academic Publishers, 2000.
Знайти повний текст джерелаPeters, Timothy Francis. Physiological effects of chronic exercise-training and hemorrhage in response to central angiotensin II administration in male rats. 1993.
Знайти повний текст джерелаFlynn, Angela Joanne. Androgenic effects on angiotensin II-induced blood pressure and cochlear blood flow changes in rats. 1990.
Знайти повний текст джерелаRoberts, Kim Alexandria. Anatomical mapping of angiotensin pathways in the central nervous system. 1993.
Знайти повний текст джерелаKing, Steven Jay. Effects of angiotensin on central and peripheral tissues involved in blood pressure homeostasis. 1986.
Знайти повний текст джерелаBatt, Carol Mohr. Use of peptidases and peptidase inhibitors to manipulate endogenous levels of angiotensin in normotensive and hypertensive rats. 1992.
Знайти повний текст джерелаFerrario, Carlos M., Mustafa F. Lokhandwala, and Joseph P. Buckley. Central Actions of Angiotensin and Related Hormones. Elsevier Science & Technology Books, 2013.
Знайти повний текст джерелаТези доповідей конференцій з теми "Angiotensins Physiological effect"
Kelesheva, L. F., T. V. Shurtakova, M. F. Obukhova та A. V. Kotov. "EFFECT OF IMMUNIZATION AGAINST ANGIOTENSIN-ΙΙ ON ALCOHOL INTAKE IN RATS". У MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-36.
Повний текст джерелаKelesheva, L. F., and E. R. Annaeva. "RELATIONSHIP BETWEEN ACTIVITY OF THE RENIN-ANGIOTENSIN SYSTEM AND RESISTANCE TO ONCE AND CHRONIC EFFECTS OF ETHANOL." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-37.
Повний текст джерела