Calcineurin-dependent induction of markers of uterine receptivity by angiotensin II in rat endometrial stromal cells. The role of the trophoblast renin-angiotensin-system

Placenta ◽  
2015 ◽  
Vol 36 (4) ◽  
pp. 498-499
Author(s):  
F. Scotto ◽  
E. Grotz ◽  
C. Parrado ◽  
L. Salaverry ◽  
T. Gentile ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Stromal Cells ◽  
Renin Angiotensin System ◽  
Uterine Receptivity ◽  
Endometrial Stromal Cells ◽  
Angiotensin System ◽  
Renin Angiotensin

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.

Effect of angiotensin II antagonist infusion on autoregulation of renal blood flow

1976 ◽  
Vol 231 (4) ◽  
pp. 1267-1271 ◽  
Author(s):  
Y Abe ◽  
T Kishimoto ◽  
K Yamamoto
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Pressure Reduction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Autoregulation ◽  
Angiotensin Ii Antagonist

The role of the renin-angiotensin system in the autoregulation of renal blood flow was examined in the anesthetized dog. The angiotensin II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, was continuously infused into the renal artery at rates of 1 and 3 mug/min, and renin secretion rate and intrarenal distribution of blood flow as well as total renal blood flow were measured during acute reductions in renal perfusion pressure within and below the range of autoregulation. Renal autoregulation and redistribution of blood flow by pressure reduction were not disturbed by the angiotensin II antagonist. This result does not provide any evidence for a primary role of the renin-angiotensin system in renal autoregulation. Redistribution of blood flow by pressure reduction occurred independently of the renin-angiotensin system. It might depend on the differences in the resting tone among the zones.

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