This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In Project 1, Kobori and associates continued studies on the mechanisms responsible for the concomitant increases in renal AGT protein and AGT mRNA in Ang II dependent hypertension. The central hypothesis of this project is that Ang II-dependent hypertension is characterized by augmented proximal tubular AGT secretion leading to increased distal nephron spillover of AGT coupled with stimulation of distal tubular renin formation leading to increased distal formation of Ang II. Furthermore, the distal nephron spillover of AGT is reflected by increased urinary AGT excretion rates, which can be used as an index of intrarenal Ang II activity.
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