Tissue kallikrein deficiency and renovascular hypertension in the mouse.

@article{GriolCharhbili2009TissueKD,
  title={Tissue kallikrein deficiency and renovascular hypertension in the mouse.},
  author={Violaine Griol‐Charhbili and Laurent Sabbah and Juliana Almada Colucci and M P Vincent and V{\'e}ronique Baudrie and Dominique Laude and Jean-Luc Elghozi and Patrick Bruneval and Nicolas Picard and Pierre Meneton and Francois Alhenc-Gelas and Christine Richer},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2009},
  volume={296 5},
  pages={
          R1385-91
        }
}
The kallikrein kinin system (KKS) is involved in arterial and renal functions. It may have an antihypertensive effect in both essential and secondary forms of hypertension. The role of the KKS in the development of two-kidneys, one-clip (2K1C) hypertension, a high-renin model, was investigated in mice rendered deficient in tissue kallikrein (TK) and kinins by TK gene inactivation (TK-/-) and in their wild-type littermates (TK+/+). Four weeks after clipping the renal artery, blood flow was… 
Antihypertensive role of tissue kallikrein in hyperaldosteronism in the mouse.
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It is shown that TK deficiency exacerbates aldosterone-salt-induced hypertension, and the study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.
Pathophysiology of genetic deficiency in tissue kallikrein activity in mouse and man.
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The beneficial effect of ACE/kininase II inhibitors or angiotensin II AT1 receptor antagonists in cardiac ischaemia is abolished in TK-deficient mice, suggesting a prominent role for TK and kinins in the cardioprotective action of these drugs.
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Antihypertensive Role of Kidney: Focus on Tissue Kallikreins
TLDR
Though KKS operates in both cardiovascular and renal systems, only the regulatory mechanisms of renal KKS on BP homeostasis has been considered for discussion in this review.
Genetic manipulation and genetic variation of the kallikrein-kinin system: impact on cardiovascular and renal diseases.
TLDR
Clinical and experimental findings from genetic manipulation of the kallikrein-kinin system (KKS) in mice, and study of human genetic variability in KKS components, have allowed recognizing the physiological role of KKS in health and in disease.
Tissue kallikrein-kinin therapy in hypertension and organ damage.
  • J. Chao, G. Bledsoe, L. Chao
  • Biology, Medicine
    Progress in drug research. Fortschritte der Arzneimittelforschung. Progres des recherches pharmaceutiques
  • 2014
TLDR
Tissue kallikrein/kinin treatment attenuates cardiovascular, renal, and brain injury by inhibiting oxidative stress, apoptosis, inflammation, hypertrophy, and fibrosis and promoting angiogenesis and neurogenesis.
A Novel Category of Anti-Hypertensive Drugs for Treating Salt-Sensitive Hypertension on the Basis of a New Development Concept
TLDR
Ebelactone B, poststatin, and KATP channel blockers could become novel antihypertensive drugs by increase in urinary kinin levels, and roles of kinin in cardiovascular diseases were discussed.
Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site.
Endogenous cardiotonic steroids, through their interaction with the ouabain-binding site of the Na-K-ATPase α-subunit, have been implicated in a variety of cardiovascular disease states including
Tissue kallikrein, blood pressure regulation, and hypertension: insight from genetic kallikrein deficiency
TLDR
Observations suggest that kallikrein can have antihypertensive function in physiological situations where sodium retention can trigger blood pressure elevation.
Danhong injection reduces vascular remodeling and up-regulates the Kallikrein-kinin system in spontaneously hypertensive rats
TLDR
The reduction of vascular remodeling and the up-regulation of Kallikrein-kinin system contribute, at least in part, to the antihypertensive effect of DHI in SHR.
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TLDR
The results indicate that kinins acting on the BK B2 receptor exert a protective action against excessive blood pressure elevation during early phases of 2K1C hypertension.
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TLDR
The concentration of vascular kininogenase in rats with one-kidney, one clip renovascular hypertension and in unilaterally nephrectomized normotensive rats was studied.
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TLDR
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TLDR
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TLDR
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TLDR
It is demonstrated that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure, and that a functional kallIKrein–kinin system is necessary for normal cardiac and arterial function in the mouse.
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TLDR
This study demonstrates the active contribution of the vascular kallikrein-kinin system to one-third of the flow-dependent dilation response via activation of B2 receptors coupled to endothelial NO release.
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