Cross-talk of the renin-angiotensin and kallikrein-kinin systems
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Bing Shen
Abstract
The renin-angiotensin (RAS) and kallikrein-kinin (KKS) systems play a key role in multiple physiological and pathophysiological conditions, including growth and development, inflammation, blood pressure regulation and control of renal function. In many instances, kinins and angiotensin II work together, e.g., during development, whereas they oppose each other's actions in the regulation of vascular tone and renal function. The RAS and KKS systems also interact at multiple levels, so that changes in the activity of one system greatly impact the activity of the other. The purpose of this brief review is to highlight recent knowledge regarding interactions at the cellular and molecular levels between the two systems, with an emphasis on the coordinate developmental regulation of these phylogenetically conserved vasoactive systems.
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©2006 by Walter de Gruyter Berlin New York
Articles in the same Issue
- Exploring the future of local vascular and inflammatory mediators
- Genetically altered animal models in the kallikrein-kinin system
- The kinin system mediates hyperalgesia through the inducible bradykinin B1 receptor subtype: evidence in various experimental animal models of type 1 and type 2 diabetic neuropathy
- Cross-talk of the renin-angiotensin and kallikrein-kinin systems
- Which endothelium-derived factors are really important in humans?
- Kinin- and angiotensin-converting enzyme (ACE) inhibitor-mediated nitric oxide production in endothelial cells
- Anti-inflammatory effects of kinins via microglia in the central nervous system
- Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma
- Three-dimensional structure of an AMPA receptor without associated stargazin/TARP proteins
- Dual antagonists of the bradykinin B1 and B2 receptors based on a postulated common pharmacophore from existing non-peptide antagonists
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- Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR)
- Cathepsin B localizes to plasma membrane caveolae of differentiating myoblasts and is secreted in an active form at physiological pH
Articles in the same Issue
- Exploring the future of local vascular and inflammatory mediators
- Genetically altered animal models in the kallikrein-kinin system
- The kinin system mediates hyperalgesia through the inducible bradykinin B1 receptor subtype: evidence in various experimental animal models of type 1 and type 2 diabetic neuropathy
- Cross-talk of the renin-angiotensin and kallikrein-kinin systems
- Which endothelium-derived factors are really important in humans?
- Kinin- and angiotensin-converting enzyme (ACE) inhibitor-mediated nitric oxide production in endothelial cells
- Anti-inflammatory effects of kinins via microglia in the central nervous system
- Platelets promote coagulation factor XII-mediated proteolytic cascade systems in plasma
- Three-dimensional structure of an AMPA receptor without associated stargazin/TARP proteins
- Dual antagonists of the bradykinin B1 and B2 receptors based on a postulated common pharmacophore from existing non-peptide antagonists
- Generation and characterization of a humanized bradykinin B1 receptor mouse
- The role of bradykinin B1 receptor on cardiac remodeling in stroke-prone spontaneously hypertensive rats (SHR-SP)
- Molecular identification and pharmacological profile of the bovine kinin B1 receptor
- Interplay of human tissue kallikrein 4 (hK4) with the plasminogen activation system: hK4 regulates the structure and functions of the urokinase-type plasminogen activator receptor (uPAR)
- Cathepsin B localizes to plasma membrane caveolae of differentiating myoblasts and is secreted in an active form at physiological pH