Enhanced renal function in bradykinin B(2) receptor transgenic mice.

@article{Wang2000EnhancedRF,
  title={Enhanced renal function in bradykinin B(2) receptor transgenic mice.},
  author={D. Z. Wang and Hideaki Yoshida and Qing Song and Lee Chao and Julie Chao},
  journal={American journal of physiology. Renal physiology},
  year={2000},
  volume={278 3},
  pages={
          F484-91
        }
}
  • D. Wang, H. Yoshida, +2 authors J. Chao
  • Published 1 March 2000
  • Biology, Medicine
  • American journal of physiology. Renal physiology
The tissue kallikrein-kinin system has been recognized as a paracrine and/or autocrine hormonal system that regulates arterial pressure, renal hemodynamics, and electrolyte excretion. We have created a transgenic mouse model overexpressing human bradykinin B(2) receptor, and the mice developed lifetime hypotension. With this animal model, we further analyzed the potential role of B(2) receptors in regulation of renal function. Baseline urinary excretion, urinary potassium excretion, and pH were… 
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Decreased renal NO excretion and reduced glomerular tuft area in mice lacking the bradykinin B2 receptor.
TLDR
Backcrossed B(2)-/- mice had normal blood pressure and normal apparent renal hemodynamics and morphology, however, reduced renal nitrite excretion and glomerular cGMP content were found, which was associated with a reducedglomerular capillary surface area.
Mechanisms of Disease: the tissue kallikrein–kinin system in hypertension and vascular remodeling
TLDR
Development of novel therapeutic approaches to bolster kinin activity in the vascular wall and in specific compartments in the kidney might be a highly effective strategy for the treatment of hypertension and its complications, including cardiac hypertrophy and renal failure.
Normal Blood Pressure and Renal Function in Mice Lacking the Bradykinin B2 Receptor
TLDR
The data suggest that the absence of B2 receptor function does not necessarily make B1 receptor knockout mice hypertensive or induce salt sensitivity, and that differences in the genetic background or an adaptation to the loss of B 2 receptor function may account for these results.
The Bradykinin B2 receptor is required for full expression of renal COX-2 and renin
Role of bradykinin in angiotensin-converting enzyme knockout mice.
TLDR
A line of mice deficient in both the B(2) receptor and ACE did not differ from ACE knockout mice in blood pressure, urine concentrating ability, renal pathology, and hematocrit, suggesting abnormalities of bradykinin accumulation do not play an important role in the ACE knockout phenotype.
Delivery of recombinant adeno-associated virus-mediated human tissue kallikrein for therapy of chronic renal failure in rats.
TLDR
Restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6-nephrectomized rats via changes in the expression and activation of G protein-coupled receptors including B(2)R.
Angiotensin-converting enzyme II in the heart and the kidney.
TLDR
ACE2 not only controls angiotensin II levels but functions as a protease on additional molecular targets that could contribute to the observed in vivo phenotypes of ACE2 mutant mice, suggesting that ACE2 seems to be a molecule that has protective roles in heart and kidney.
Cross talk between kinin and angiotensin II receptors in mouse abdominal aorta
TLDR
It is concluded that cross talk between kinin and AngII receptors occurs in mouse abdominal aorta and that both peptides may regulate the initiation and progression of important pathophysiological processes, such as hypertension and inflammation.
Angiotensin II–Induced Hypertension in Bradykinin B2 Receptor Knockout Mice
TLDR
It is demonstrated that the kallikrein-kinin system selectively buffers the vasoconstrictor activity of Ang II, and the enhanced susceptibility of B2R−/− mice to Ang II–induced hypertension and renal vasconstriction is likely due to an impaired ability to release NO by endogenous kinins.
Angiotensin II – Induced Hypertension in Bradykinin B 2 Receptor Knockout Mice
TLDR
It is demonstrated that the kallikrein-kinin system selectively buffers the vasoconstrictor activity of Ang II and the enhanced susceptibility of B2R 2/2 mice to Ang II–induced hypertension and renal vasconstriction is likely due to an impaired ability to release NO by endogenous kinins.
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