Glomerular hyperfiltration (GH) is an important mechanism in the development of albuminuria in hypertension. The Munich Wistar Frömter (MWF) rat is a non-diabetic model of chronic kidney disease (CKD) with GH due to inherited low nephron number resulting in spontaneous albuminuria and podocyte injury. In MWF rats, we identified prostaglandin (PG) E (PGE) signaling as a potential causative mechanism of albuminuria in GH.
View Article and Find Full Text PDFBackground: Glomerular hyperfiltration (GH) is an important mechanism in the development of albuminuria in hypertension. Upregulation of COX2 (cyclooxygenase 2) and prostaglandin E (PGE) was linked to podocyte damage in GH. We explored the potential renoprotective effects of either separate or combined pharmacological blockade of EP2 (PGE receptor type 2) and EP4 (PGE receptor type 4) in GH.
View Article and Find Full Text PDFAims: Prostaglandins are important signaling lipids with prostaglandin E (PGE) known to be the most abundant prostaglandin across tissues. In kidney, PGE plays an important role in the regulation of kidney homeostasis through its EP receptor signaling. Catabolism of PGE yields the metabolic products that are widely considered biologically inactive.
View Article and Find Full Text PDFGlomerular hyperfiltration is an important mechanism in the development of albuminuria. During hyperfiltration, podocytes are exposed to increased fluid flow shear stress (FFSS) in Bowman's space. Elevated Prostaglandin E2 (PGE) synthesis and upregulated cyclooxygenase 2 (Cox2) are associated with podocyte injury by FFSS.
View Article and Find Full Text PDFThe Ussing chamber is an old but still powerful technique originally designed to study the vectorial transport of ions through frog skin. This technique is also used to investigate the transport of chemical agents through the intestinal barrier as well as drug metabolism in enterocytes, both of which are key determinants for the bioavailability of orally administered drugs. More contemporary model systems, such as Caco-2 cell monolayers or stably transfected cells, are more limited in their use compared to the Ussing chamber because of differences in expression rates of transporter proteins and/or metabolizing enzymes.
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