Role of the Renin-angiotensin System (RAS) Inhibition in Chronic Aortic Regurgitation (AR) Using Angiotensin II Type1a Receptor Knockout Mice

2005 ◽  
Vol 11 (9) ◽  
pp. S318
Author(s):  
Michio Nakanishi ◽  
Masaki Harada ◽  
Koichiro Kuwahara ◽  
Rika Kawakami ◽  
Yasuaki Nakagawa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Aortic Regurgitation ◽  
Knockout Mice ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ras Inhibition ◽  
Chronic Aortic Regurgitation

Is angiotensin essential in drinking induced by water deprivation and caval ligation?

1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Essential Role ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.

Role of the renin-angiotensin system in the pathogenesis of preeclampsia

2005 ◽  
Vol 288 (4) ◽  
pp. F614-F625 ◽  
Author(s):  
Dinesh M. Shah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Receptor Activation ◽  
Gravid Uterus ◽  
Type I ◽  
Hypertensive Disorder ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

Preeclampsia is a hypertensive disorder unique to pregnancy with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped “kidney” and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidence of the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT1) receptor activation. Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1and bradykinin B2receptor heterodimerization and the production of an autoantibody against AT1. Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.

Role of the tissue renin-angiotensin system in the response of the rat adrenal to exogenous angiotensin II.

1996 ◽  
Vol 22 (4) ◽  
pp. 589-593 ◽  
Author(s):  
G. P. Vinson ◽  
R. Teja ◽  
M. M. Ho ◽  
J. P. Hinson ◽  
J. R. Puddefoot
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Trophic effects of potassium loading on the rat zona glomerulosa: permissive role of ACTH and angiotensin II

1985 ◽  
Vol 108 (1) ◽  
pp. 98-103 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Piera Rebuffat ◽  
Claudia Robba ◽  
Ludwig K. Malendowicz ◽  
Gastone G. Nussdorfer
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Zona Glomerulosa ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Trophic Effects ◽  
Potassium Loading ◽  
Permissive Role ◽  
Trophic Action

Abstract. The trophic effects of chronic potassium loading on the rat zona glomerulosa were investigated by morphometric and radioimmunological methods. Potassium loading exerted a potent adrenoglomerulotrophic effect in saline treated control rats, but it was not able to reverse the captopril- and dexamethasone-induced atrophy of the zona glomerulosa. However, if the captopril/dexamethasone administered rats were given maintenance doses of angiotensin II and ACTH, potassium loading was found to exert a strong trophic action. The hypothesis is advanced that potassium loading requires the integrity of both the renin-angiotensin system and the hypothalamo-hypophyseal axis to exert its powerful direct stimulating effect on the growth and steroidogenic capacity of the rat zona glomerulosa.

Measurement of the Renin-Angiotensin System in Heart Failure

2000 ◽  
Vol 1 (3) ◽  
pp. 210-226 ◽  
Author(s):  
Shann Dixon Kim
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Advantages And Disadvantages ◽  
Angiotensin I Converting Enzyme

Angiotensin II (ANG II), the effector hormone of the renin-angiotensin system (RAS), has been implicated in the pathophysiology and progression of heart failure. Therefore, the measurement of ANGII has become important to characterize the role of this neurohormone in heart failure. However, because ANG II has been difficult to measure, other components of the RAS have been measured to characterize ANG II production. The RAS components (e.g., renin, angiotensin I–converting enzyme [ACE], angiotensin II) have been measured with a variety of techniques. In this review, RAS physiology and the techniques used to measure the RAS components are discussed. In addition, the advantages and disadvantages of the RAS measurement methods are described.

scholarly journals Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury

2019 ◽  
Vol 30 (12) ◽  
pp. 2307-2320 ◽  
Author(s):  
Kazunori Inoue ◽  
Xuefei Tian ◽  
Heino Velazquez ◽  
Keita Soda ◽  
Zhen Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Knockout Mice ◽  
Renin Angiotensin System ◽  
Membrane Dynamics ◽  
Receptor Type ◽  
Angiotensin Ii Receptor ◽  
Double Knockout ◽  
Angiotensin System ◽  
Renin Angiotensin

BackgroundInhibition of the renin-angiotensin system remains a cornerstone in reducing proteinuria and progression of kidney failure, effects believed to be the result of reduction in BP and glomerular hyperfiltration. However, studies have yielded conflicting results on whether podocyte-specific angiotensin II (AngII) signaling directly induces podocyte injury. Previous research has found that after AngII stimulation, β-arrestin–bound angiotensin II receptor type 1 (AT1R) is internalized in a clathrin- and dynamin-dependent manner, and that Dynamin1 and Dynamin2 double-knockout mice exhibit impaired clathrin-mediated endocytosis.MethodsWe used podocyte-specific Dyn double-knockout mice to examine AngII-stimulated AT1R internalization and signaling in primary podocytes and controls. We also examined the in vivo effect of AngII in these double-knockout mice through renin-angiotensin system blockers and through deletion of Agtr1a (which encodes the predominant AT1R isoform expressed in kidney, AT1aR). We tested calcium influx, Rac1 activation, and lamellipodial extension in control and primary podocytes of Dnm double-knockout mice treated with AngII.ResultsWe confirmed augmented AngII-stimulated AT1R signaling in primary Dnm double-knockout podocytes resulting from arrest of clathrin-coated pit turnover. Genetic ablation of podocyte Agtr1a in Dnm double-knockout mice demonstrated improved albuminuria and kidney function compared with the double-knockout mice. Isolation of podocytes from Dnm double-knockout mice revealed abnormal membrane dynamics, with increased Rac1 activation and lamellipodial extension, which was attenuated in Dnm double-knockout podocytes lacking AT1aR.ConclusionsOur results indicate that inhibiting aberrant podocyte-associated AT1aR signaling pathways has a protective effect in maintaining the integrity of the glomerular filtration barrier.

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