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Homeostasis and Tubuloglomerular Feedback

稳态和肾小球反馈

基本信息

批准号：
8974225
负责人：
SCOTT Culver THOMSON
金额：
--
依托单位：
VA SAN DIEGO HEALTHCARE SYSTEM
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-04-01 至 2017-09-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8974225
关键词：
Affect Body Fluids Cardiovascular Diseases Chronic Kidney Failure Cicatrix Communication Data Diet End stage renal failure Engineering Equilibrium Event Exposure to Feedback Flowmetry Funding Future Glomerular Capillary Goals Grant Health Homeostasis Injury Juxtaglomerular Apparatus Kidney Logic Maps Metabolic Methods Micropuncture Mission Modeling Modus N-Methyl-D-Aspartate Receptors Nephrectomy Nephrons Nitric Oxide Patient Care Patients Physiology Plant Roots Process Rattus Records Regulation Relaxation Renal Blood Flow Renal function Research Risk Factors Role Sentinel Series Signal Transduction Speed Staging Stretching System Time Tissues Tubular formation Ursidae Family Veterans Work career development clinically relevant control theory design dietary salt feeding glomerular filtration glomerular function hemodynamics high salt diet improved in vivo interest kidney metabolism novel research study response salt balance salt intake tool

项目摘要

DESCRIPTION (provided by applicant): Chronic kidney disease (CKD) is the precursor to most end-stage renal failure and is a potent risk factor for cardiovascular disease. Recent interest in CKD has focused on processes of structural change that occur later in the course of CKD when functioning kidney is replaced by scar tissue. We ascribe to the view that these processes begin as adaptive mechanisms, rooted in physiology, to compensate for an earlier injury, then go awry because the means to control them is lost. It is the general purpose of the proposed research to investigate cardinal features of kidney physiology early in the course of CKD by applying renal micropuncture methods in a standard model for early CKD, namely subtotal nephrectomy (STN) in the rat. We have discovered that feeding high NaCl diet to a rat during the first week after STN leads to a reversal of the tubuloglomerular feedback (TGF) response from negative to positive gain. While this will speed up the return to salt balance, it also signifies that the kidney is willing to forego the functional and hemodynamic stability normally conferred by TGF. This shift to anomalous TGF establishes a positive relationship between dietary salt intake and dynamic stretch-relaxation of the glomerular capillary wall, which may explain the nefarious effect of dietary salt in CKD. The upcoming research will determine whether this physiology remains relevant beyond the early stages of adaptation to nephron loss, whether it is a durable process that persists after high NaCl is withdrawn, whether it depends on Na, Cl, or both, and how it interacts with kidney metabolism.

描述（由申请人提供）：