scholarly journals Kinin B1 receptor antagonism is equally efficient as angiotensin receptor 1 antagonism in reducing renal fibrosis in experimental obstructive nephropathy, but is not additive

2015 ◽  
Vol 6 ◽  
Author(s):  
Antoine Huart ◽  
Julie Klein ◽  
Julien Gonzalez ◽  
Bénédicte Buffin-Meyer ◽  
Eric Neau ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Obstructive Nephropathy ◽  
Angiotensin Receptor ◽  
Receptor Antagonism ◽  
B1 Receptor ◽  
Kinin B1 Receptor

scholarly journals Renal fibrosis due to multiple cisplatin treatment is exacerbated by kinin B1 receptor antagonism

2021 ◽  
Vol 54 (12) ◽  
Author(s):  
A. Budu ◽  
L.C. Freitas-Lima ◽  
A.C. de Arruda ◽  
M.S. Perilhão ◽  
J. Barrera-Chimal ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Receptor Antagonism ◽  
B1 Receptor ◽  
Kinin B1 Receptor

scholarly journals Delayed blockade of the kinin B1 receptor reduces renal inflammation and fibrosis in obstructive nephropathy

2008 ◽  
Vol 23 (1) ◽  
pp. 134-142 ◽  
Author(s):  
J. Klein ◽  
J. Gonzalez ◽  
J. Duchene ◽  
L. Esposito ◽  
J. P. Pradere ◽  
...  
Keyword(s):  
Obstructive Nephropathy ◽  
Renal Inflammation ◽  
B1 Receptor ◽  
Kinin B1 Receptor

scholarly journals Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons

2020 ◽  
Vol 22 (1) ◽  
pp. 145
Author(s):  
Rohan Umesh Parekh ◽  
Srinivas Sriramula
Keyword(s):  
Protein Expression ◽  
Renin Angiotensin System ◽  
Neuronal Cultures ◽  
Wild Type ◽  
High Concentration ◽  
Neurogenic Hypertension ◽  
B1 Receptor ◽  
Gene And Protein Expression ◽  
Kinin B1 Receptor ◽  
Specific Antagonist

Angiotensin converting enzyme 2 (ACE2) is a critical component of the compensatory axis of the renin angiotensin system. Alterations in ACE2 gene and protein expression, and activity mediated by A Disintegrin And Metalloprotease 17 (ADAM17), a member of the “A Disintegrin And Metalloprotease” (ADAM) family are implicated in several cardiovascular and neurodegenerative diseases. We previously reported that activation of kinin B1 receptor (B1R) in the brain increases neuroinflammation, oxidative stress and sympathoexcitation, leading to the development of neurogenic hypertension. We also showed evidence for ADAM17-mediated ACE2 shedding in neurons. However, whether kinin B1 receptor (B1R) activation has any role in altering ADAM17 activity and its effect on ACE2 shedding in neurons is not known. In this study, we tested the hypothesis that activation of B1R upregulates ADAM17 and results in ACE2 shedding in neurons. To test this hypothesis, we stimulated wild-type and B1R gene-deleted mouse neonatal primary hypothalamic neuronal cultures with a B1R-specific agonist and measured the activities of ADAM17 and ACE2 in neurons. B1R stimulation significantly increased ADAM17 activity and decreased ACE2 activity in wild-type neurons, while pretreatment with a B1R-specific antagonist, R715, reversed these changes. Stimulation with specific B1R agonist Lys-Des-Arg9-Bradykinin (LDABK) did not show any effect on ADAM17 or ACE2 activities in neurons with B1R gene deletion. These data suggest that B1R activation results in ADAM17-mediated ACE2 shedding in primary hypothalamic neurons. In addition, stimulation with high concentration of glutamate significantly increased B1R gene and protein expression, along with increased ADAM17 and decreased ACE2 activities in wild-type neurons. Pretreatment with B1R-specific antagonist R715 reversed these glutamate-induced effects suggesting that indeed B1R is involved in glutamate-mediated upregulation of ADAM17 activity and ACE2 shedding.

scholarly journals Up-regulation of kinin B1 receptor in the lung of streptozotocin-diabetic rat: autoradiographic and functional evidence

2003 ◽  
Vol 138 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Rose Mari J Vianna ◽  
Brice Ongali ◽  
Domenico Regoli ◽  
João Batista Calixto ◽  
Réjean Couture
Keyword(s):  
Diabetic Rat ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Streptozotocin Diabetic Rat

Agonist Activity at the Kinin B1 Receptor:  Structural Requirements of the Central Tetrapeptide

2001 ◽  
Vol 44 (2) ◽  
pp. 274-278 ◽  
Author(s):  
Paolo Rovero ◽  
Maria Pellegrini ◽  
Armida Di Fenza ◽  
Stefania Meini ◽  
Laura Quartara ◽  
...  
Keyword(s):  
Agonist Activity ◽  
Structural Requirements ◽  
B1 Receptor ◽  
Kinin B1 Receptor

scholarly journals The Role of Apelin on the Alleviative Effect of Angiotensin Receptor Blocker in Unilateral Ureteral Obstruction-Induced Renal Fibrosis

Nephron Extra ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Masashi Nishida ◽  
Yasuko Okumura ◽  
Tatsujiro Oka ◽  
Kentaro Toiyama ◽  
Seiichiro Ozawa ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Angiotensin Receptor Blocker ◽  
Unilateral Ureteral Obstruction ◽  
Receptor Blocker ◽  
Angiotensin Receptor

Obstructive nephropathy and renal fibrosis

2002 ◽  
Vol 283 (5) ◽  
pp. F861-F875 ◽  
Author(s):  
Saulo Klahr ◽  
Jeremiah Morrissey
Keyword(s):  
Renal Disease ◽  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Rodent Model ◽  
Renal Diseases ◽  
Obstructive Nephropathy ◽  
Therapeutic Approaches ◽  
Cellular Events ◽  
The Impact ◽  
Made In

Interstitial fibrosis has a major role in the progression of renal diseases. Several animal models are available for the study of renal fibrosis. The models of aminonucleoside-induced nephrotic syndrome, cyclosporin nephrotoxicity, and passive Heyman nephritis are characterized by molecular and cellular events similar to those that occur in obstructive nephropathy. Additionally, inhibition of angiotensin-converting enzyme exerts salutary effects on the progression of renal fibrosis in obstructive nephropathy. Unilateral ureteral obstruction (UUO) has emerged as an important model for the study of the mechanisms of renal fibrosis and also for the evaluation of the impact of potential therapeutic approaches to ameliorate renal disease. Many quantifiable pathophysiological events occur over the span of 1 wk of UUO, making this an attractive model for study. This paper reviews some of the ongoing studies that utilized a rodent model of UUO. Some of the findings of the animal model have been compared with observations made in patients with obstructive nephropathy. Most of the evidence suggests that the rodent model of UUO is reflective of human renal disease processes.

Blockade of sensory abnormalities and kinin B1 receptor expression by N-Acetyl-l-Cysteine and ramipril in a rat model of insulin resistance

2008 ◽  
Vol 589 (1-3) ◽  
pp. 66-72 ◽  
Author(s):  
Mahmoud Ali Ismael ◽  
Sébastien Talbot ◽  
Cynthia L. Carbonneau ◽  
Christian M. Beauséjour ◽  
Réjean Couture
Keyword(s):  
Insulin Resistance ◽  
Rat Model ◽  
Receptor Expression ◽  
Sensory Abnormalities ◽  
B1 Receptor ◽  
Kinin B1 Receptor
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