scholarly journals A Possible Anti-Inflammatory Role of Angiotensin II Type 2 Receptor in Immune-Mediated Glomerulonephritis during Type 1 Receptor Blockade

2006 ◽  
Vol 169 (5) ◽  
pp. 1577-1589 ◽  
Author(s):  
Hirokazu Okada ◽  
Tsutomu Inoue ◽  
Tomohiro Kikuta ◽  
Yusuke Watanabe ◽  
Yoshihiko Kanno ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Anti Inflammatory

Angiotensin II type 1 receptor blockade attenuates renal fibrogenesis in an immune-mediated nephritic kidney through counter-activation of angiotensin II type 2 receptor

2004 ◽  
Vol 314 (2) ◽  
pp. 403-408 ◽  
Author(s):  
Hirokazu Okada ◽  
Yusuke Watanabe ◽  
Tsutomu Inoue ◽  
Tatsuya Kobayashi ◽  
Tomohiro Kikuta ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Renal Fibrogenesis

scholarly journals Possible Role of TGF – B Pathways in Schizophrenia / Moguća Uloga TTGF - B Signalnih Puteva U Shizofreniji

2016 ◽  
Vol 17 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Milica Borovcanin ◽  
Ivan Jovanovic ◽  
Slavica Djukic Dejanovic ◽  
Gordana Radosavljevic ◽  
Nebojsa Arsenijevic ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Psychotic Episode ◽  
T Helper ◽  
Helper Cell Type ◽  
State Marker ◽  
Valuable Marker ◽  
Anti Inflammatory

AbstractThe phenomenological uniqueness of each patient with schizophrenia is determined by complex symptomatology, particularly the overlapping of symptoms and their prominence in certain phases of this mental disorder. Establishing biological markers is an important step in the further objectivisation and quantification of schizophrenia. Identifying the cytokine profiles that precede a psychotic episode could direct the strategies for relapse prevention and be useful in predicting disease progression and treatment response. In the context of infl ammation, TGF-β exerts potent anti-inflammatory and immunosuppressive functions by inhibiting pro-inflammatory cytokine synthesis, but it can also have pro-inflammatory functions through its stimulatory effects on inflammatory Th17 cells. It has been shown that the T helper cell type-1 and type-17 responses are reduced and type-2 response is increased in patients with schizophrenia. Both data from the literature and our results also indicate the presence of an anti-inflammatory response through production of the TGF-β regulatory cytokine. A meta-analysis of plasma cytokine alterations suggested that TGF-β is the state marker for acute exacerbation of schizophrenia, and we showed that TGF-β can also be a valuable marker for psychosis. Hyperactivity of TGF-β signalling pathways in schizophrenia may be both a neuroprotective mechanism and a possible therapeutic target.

scholarly journals Role of angiotensin II type 2 receptors and kinins in the cardioprotective effect of angiotensin II type 1 receptor antagonists in rats with heart failure

2004 ◽  
Vol 43 (8) ◽  
pp. 1473-1480 ◽  
Author(s):  
Yun-He Liu ◽  
Xiao-Ping Yang ◽  
Edward G. Shesely ◽  
Steadman S. Sankey ◽  
Oscar A. Carretero
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardioprotective Effect ◽  
Receptor Antagonists

Angiotensin II type 2 receptor (AT2R) in renal and cardiovascular disease

2016 ◽  
Vol 130 (15) ◽  
pp. 1307-1326 ◽  
Author(s):  
Bryna S.M. Chow ◽  
Terri J. Allen
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Cellular Growth ◽  
Receptor Subtype ◽  
Electrolyte Balance ◽  
Ang Ii ◽  
Biological Responses

Angiotensin II (Ang II) is well-considered to be the principal effector of the renin–angiotensin system (RAS), which binds with strong affinity to the angiotensin II type 1 (AT1R) and type 2 (AT2R) receptor subtype. However, activation of both receptors is likely to stimulate different signalling mechanisms/pathways and produce distinct biological responses. The haemodynamic and non-haemodynamic effects of Ang II, including its ability to regulate blood pressure, maintain water–electrolyte balance and promote vasoconstriction and cellular growth are well-documented to be mediated primarily by the AT1R. However, its biological and functional effects mediated through the AT2R subtype are still poorly understood. Recent studies have emphasized that activation of the AT2R regulates tissue and organ development and provides in certain context a potential counter-regulatory mechanism against AT1R-mediated actions. Thus, this review will focus on providing insights into the biological role of the AT2R, in particular its actions within the renal and cardiovascular system.

scholarly journals Renal effects of angiotensin II in the newborn period: role of type 1 and type 2 receptors

2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Angela E. Vinturache ◽  
Francine G. Smith
Keyword(s):  
Angiotensin Ii ◽  
Newborn Period ◽  
Renal Effects

Angiotensin II mediates uterine vasoconstriction through α-stimulation

2004 ◽  
Vol 287 (1) ◽  
pp. H126-H134 ◽  
Author(s):  
Blair E. Cox ◽  
Timothy A. Roy ◽  
Charles R. Rosenfeld
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Pressor Responses ◽  
Adrenergic Activation

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intra-arterial infusions do not. Type 2 ANG II (AT2) receptors predominate in uterine vascular smooth muscle; this may reflect involvement of systemic type 1 ANG II (AT1) receptor-mediated α-adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine α-receptor blockade and in the absence or presence of AT1 receptor blockade in pregnant and nonpregnant ewes. Systemic α-receptor blockade inhibited phenylephrine-mediated increases in mean arterial pressure (MAP) and UVR, whereas uterine α-receptor blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine α-receptor blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT1 receptor blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT1 receptor blockade + systemic α-receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT2 receptor blockade had no effects. We have shown that ANG II-mediated pressor responses reflect activation of systemic vascular AT1 receptors, whereas increases in UVR reflect AT1 receptor-mediated release of an α-agonist and uterine autoregulatory responses.

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