Publications by authors named "Robert Repetti"
Dyslipidemia, with changes in plasma membrane (PM) composition, is associated with hypertension, while rising PM cholesterol induces Na channel activity. We hypothesize that ablation of renal tubular ABCA1, a cholesterol efflux protein, leads to cholesterol- and Na-dependent changes in blood pressure (BP). Transgenic mice () expressing a doxycycline (dox)-inducible CRE recombinase were bred with mice expressing floxed ABCA1 to generate renal tubules deficient in ABCA1 (ABCA1FF).
View Article and Find Full Text PDFNephron loss initiates compensatory hemodynamic and cellular effects on the remaining nephrons. Increases in single nephron glomerular filtration rate and tubular flow rate exert higher fluid shear stress (FSS) on tubules. In principal cell (PC) culture models FSS induces ERK, and ERK is implicated in the regulation of transepithelial sodium (Na) transport, as well as, proliferation.
View Article and Find Full Text PDFCellular cholesterol modifies flow-mediated gene expression.
Am J Physiol Renal Physiol
October 2019
Article Synopsis
- Downregulation of HO-1, COX2, and NOS2 in Dahl rodents leads to salt sensitivity, but restoring these proteins improves sodium excretion and lowers blood pressure.
- Cholesterol loading in kidney collecting duct cells reduces the flow-induced activation of these important genes, suggesting that cholesterol may hinder the body's ability to excrete sodium effectively.
- Experiments show that mice on a cholesterol diet have lower urine output and altered electrolyte levels, indicating that excess cholesterol can negatively impact kidney function and sodium regulation.