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Mediation of tubuloglomerular feedback by adenosine: Evidence from mice lacking adenosine 1 receptors
TLDR
A1AR null mutant mice are a promising tool to study the functional role of A1AR in different target tissues and suggest that adenosine is a required constituent of the juxtaglomerular signaling pathway. Expand
Renal function in mice with targeted disruption of the A isoform of the Na-K-2Cl co-transporter.
TLDR
Coexpression of both high- and low-affinity isoforms of NKCC2 may permit transport and Cl-dependent tubuloglomerular feedback regulation to occur over a wider Cl concentration range and activity seems to be required for MD salt sensing in the high Cl concentrationrange. Expand
Impairment of tubuloglomerular feedback regulation of GFR in ecto-5'-nucleotidase/CD73-deficient mice.
TLDR
It is concluded that the generation of adenosine at the glomerular pole depends to a major extent on e-5'NT/CD73-mediated dephosphorylation of 5'-AMP, presumably generated from released ATP. Expand
Localization of PEPT1 and PEPT2 proton-coupled oligopeptide transporter mRNA and protein in rat kidney.
TLDR
The results conclusively demonstrate that although PEPT1 is expressed in early regions of the proximal tubule (pars convoluta), P EPT2 is specific for the latter regions of proximal Tubule ( pars recta). Expand
Tubular Localization and Tissue Distribution of Peptide Transporters in Rat Kidney
TLDR
Contrary to current opinion, the data suggest that peptides are handled in a sequential manner in proximal regions of the nephron, first by the low-affinity, high-capacity transport system and second by the high-Affinity, low- capacity transport system. Expand
MAPK Mediation of Hypertonicity-stimulated Cyclooxygenase-2 Expression in Renal Medullary Collecting Duct Cells*
TLDR
All three members of the MAPK family (ERK, JNK-2, and p38) as well as Src kinases are required for tonicity-stimulated COX-2 expression in mouse collecting duct cells and that COx-2 may play a role in cell survival of medullary cells under hypertonic conditions is concluded. Expand
Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.
TLDR
The marked elevation of GFR in diabetic mice that lack a TGF response indicates that TGF is not required to cause hyperfiltration in the Akita model of diabetes, and an A1AR-dependent mechanism, possibly TGF, limits the degree of diabetichyperfiltration and nephropathy. Expand
Fluid reabsorption in proximal convoluted tubules of mice with gene deletions of claudin-2 and/or aquaporin1.
TLDR
Aided by a fall in filtered load, the capacity of non-AQP1-dependent transcellular reabsorption is sufficient to maintain PFR without AQP1 and claudin-2 at 75% of control and is consistent with an up to 25% paracellular contribution to PFR. Expand
Impaired Glucose Tolerance in the Absence of Adenosine A1 Receptor Signaling
TLDR
ADO/A1AR signaling contributes importantly to insulin-controlled glucose homeostasis and insulin sensitivity in C57BL/6 mice and is involved in the metabolic regulation of adipose tissue. Expand
Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice.
TLDR
It is concluded that the severity of hypertension and renal failure in COX-2-deficient mice is influenced by genetic background and gender, whereas the incomplete maturation of outer cortical nephrons appears to be independent of genetic background effects. Expand
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