Regular ArticleSalt-Sensitive Hypertension in Bradykinin B2Receptor Knockout Mice☆
References (0)
Cited by (112)
Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin
2015, Vitamins and HormonesVasopressor meets vasodepressor: The AT1-B2 receptor heterodimer
2014, Biochemical PharmacologyVascular mechanisms involved in angiotensin II-induced venoconstriction in hypertensive rats
2011, PeptidesCitation Excerpt :The kalikrein–kinin system plays an important role in the maintenance of cardiovascular homeostasis. In this regard, the kinin B2R null mice present high sensitivity to hypertensive stimuli [1,5], impairment of endothelium-dependent vasodilation and decrease in NO bioavailability [15]. Moreover, studies have indicated the existence of functional interactions between angiotensin and kinin receptors in vascular cells.
Role of vascular Kinin B <inf>1</inf> and B <inf>2</inf> receptors in endothelial nitric oxide metabolism
2011, PeptidesCitation Excerpt :Mice with a targeted deletion of the gene for the B1 receptor (B1−/−) are described to be healthy, fertile and normotensive, but exhibit blunted responses to bacterial lipopolysaccharide injection and hypoalgesia [30]. Under physiological conditions, B2 receptor knockout mice (B2−/−) present normal development [9], renal hemodynamics and salt balance [2,26,35]. Nevertheless, data regarding the effects of B2 receptor deletion on blood pressure regulation are controversial.
- ☆
Abbreviations: K-K, kallikrein-kinin; ACE, angiotensin-converting enzyme; BP, blood pressure; Ang II, angiotensin II; BK, bradykinin; B2-KO, bradykinin B2receptor knockout mouse; Ach, acetylcholine.