PAF-induced kinin B1 receptor in vivo up-regulation: involvement of distinct kinase pathways

2007 ◽  
Vol 56 (S3) ◽  
pp. S488-S491
Author(s):  
Elizabeth S. Fernandes ◽  
Rodrigo Medeiros ◽  
Maria M. Campos ◽  
Joao B. Calixto
Keyword(s):  
B1 Receptor ◽  
Kinin B1 Receptor

Kinin B1 receptor-mediated motor responses in normal or inflamed rat urinary bladder in vivo

1999 ◽  
Vol 80 (1-2) ◽  
pp. 41-47 ◽  
Author(s):  
Alessandro Lecci ◽  
Stefania Meini ◽  
Manuela Tramontana ◽  
Sandro Giuliani ◽  
Marco Criscuoli ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Rat Urinary Bladder ◽  
Motor Responses ◽  
B1 Receptor ◽  
Kinin B1 Receptor

Doxorubicin cardiomyopathy-induced inflammation and apoptosis are attenuated by gene deletion of the kinin B1 receptor

2008 ◽  
Vol 389 (6) ◽  
Author(s):  
Dirk Westermann ◽  
Olga Lettau ◽  
Meike Sobirey ◽  
Alexander Riad ◽  
Michael Bader ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Cardiac Dysfunction ◽  
Cardiac Tissue ◽  
Mrna Levels ◽  
Western Blots ◽  
Cardiac Inflammation ◽  
Akt Activation ◽  
B1 Receptor ◽  
Kinin B1 Receptor

Abstract Clinical use of the anthracycline doxorubicin (DOX) is limited by its cardiotoxic effects, which are attributed to the induction of apoptosis. To elucidate the possible role of the kinin B1 receptor (B1R) during the development of DOX cardiomyopathy, we studied B1R knockout mice (B1R-/-) by investigating cardiac inflammation and apoptosis after induction of DOX-induced cardiomyopathy. DOX control mice showed cardiac dysfunction measured by pressure-volume loops in vivo. This was associated with a reduced activation state of AKT, as well as an increased bax/bcl2 ratio in Western blots, indicating cardiac apoptosis. Furthermore, mRNA levels of the proinflammatory cytokine interleukin 6 were increased in the cardiac tissue. In DOX B1R-/- mice, cardiac dysfunction was improved compared to DOX control mice, which was associated with normalization of the bax/bcl-2 ratio and interleukin 6, as well as AKT activation state. These findings suggest that B1R is detrimental in DOX cardiomyopathy in that it mediates the inflammatory response and apoptosis. These insights might have useful implications for future studies utilizing B1R antagonists for treatment of human DOX cardiomyopathy.

In vivo footprinting analysis of the human kinin B1 receptor gene promoter

2000 ◽  
Vol 28 (5) ◽  
pp. A264-A264
Author(s):  
D. Bachvarov ◽  
M. Angers ◽  
M. Bachvarova ◽  
I. Paradis ◽  
F. Marceau ◽  
...  
Keyword(s):  
Receptor Gene ◽  
Gene Promoter ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
In Vivo Footprinting

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

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

Abstract MP06: Kinin B1 Receptor Mediates Orexin System Hyperactivity In Salt-sensitive Hypertension

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Rohan U Parekh ◽  
Abdel A Abdel-rahman ◽  
Srinivas Sriramula
Keyword(s):  
Radio Telemetry ◽  
Mrna Levels ◽  
Wild Type ◽  
Salt Treatment ◽  
Neurogenic Hypertension ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Salt Sensitive Hypertension ◽  
The Brain

Hyperactivity of the orexin system contributes to several animal models of hypertension and enhances arginine vasopressin (AVP) release. We previously reported higher neuronal kinin B1 receptor (B1R) expression and brain AVP levels in hypertensive mice. However, the role of B1R and its interaction with orexin system in neurogenic hypertension have not been studied. In the present study, we tested the hypothesis that kinin B1R contributes to hypertension by upregulation of orexin-AVP signaling in the brain. Deoxycorticosterone acetate (DOCA)-salt treatment (1 mg/g body weight DOCA, 1% saline in drinking water, 3 weeks) of wild-type (WT) male mice produced a significant increase in mean arterial pressure (MAP; radio-telemetry) (138 ±3 mmHg, n=8, p<0.01) that was blunted in B1R knockout mice (121±2 mmHg, P <0.05 vs. WT+DOCA). In WT mice, DOCA-salt, compared to vehicle, increased mRNA levels of orexin receptor 1 (2.5 fold, n=9, p<0.001), orexin receptor 2 (3 fold, n=9, p<0.001) and AVP (3 fold, n=9, p<0.01) in the hypothalamic paraventricular nucleus (PVN), and these DOCA-salt evoked effects were attenuated in B1RKO mice. Similarly, DOCA-salt evoked increases in protein expression of orexin receptor 1 and 2 in the hypothalamic PVN of WT mice were attenuated by 25±5% and 33±5% (p<0.05), respectively, in B1RKO vs WT+DOCA mice. Furthermore, DOCA-salt treatment increased plasma AVP levels in WT mice compared to vehicle treated mice (13.69±1.1 vs. 47.86±8.7 pg/ml, p<0.05), but not in B1RKO mice. Together, these data provide novel evidence that kinin B1R plays an important role in mediating DOCA-salt induced hypertension possibly via upregulating the orexin-AVP signaling in the brain.

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