Virtuous Ten Studio License

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Virtuous Ten Studio.[unreadable] Chronic stimulationof the renin angiotensin aldosterone system (RAAS) is
central to a host of cardiovascular and renal
pathophysiologic conditions. This proposal centers on anovel signaling mechanism of the RAAS in cardiorenal
protection. It postulates that activation of proteaseactivated receptor 4 (PAR4) via the bradykinin (BK) 2
receptor causes a cardiorenal protective mechanism insepsis and acute kidney injury. This hypothesis is

1/4based on genetic deletion studies in mice of PAR4 andthe BK receptor in which both PAR4 and the BK
receptor confer both cardiorenal protection andthrombotic phenotype. This proposal will test thisworking hypothesis in sepsis and acute kidney injury. I
will examine the role of a recently identified G protein
coupled receptor (GPCR) termed PAR4 in thrombotic
and cardiorenal response to experimental acute kidney
injury and sepsis. I will use a bradykinin 2 (B2)
receptor knockout mice which is genetically deficientin the expression of PAR4 to assess the relative
importance of the PAR4-BK2 receptor system in the
response to acute kidney injury and sepsis. In addition,
I will use a PAR4 deficiency in the bradykinin 1
receptor knockout mice (PAR4D) to evaluate therelative importance of PAR4 and the BK receptors in
the cardiac and vascular response to acute kidney
injury and sepsis. I propose three specific aims: 1) To
characterize the response of septic PAR4D mice tocardiorenal injury. 2) To characterize the response of
septic B2 receptor knockout mice to cardiorenal
injury. 3) To characterize the response of PAR4D
mice to acute kidney injury. A better understanding of

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these pathways and their interaction may lead to more
effective therapies for cardiorenal disease.
[unreadable] [unreadable] [unreadable]Innovation and

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Virtuous Ten Studio License