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Inhibition of COX-1 attenuates the formation of thromboxane A2 and ameliorates the acute decrease in glomerular filtration rate in endotoxemic mice.
Am J Physiol Renal Physiol
August 2015
Institute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany
Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity on lipopolysaccharide (LPS)-induced renal TxA2 formation, and on endotoxemia-induced AKI in mice. Injection of LPS (3 mg/kg ip) decreased glomerular filtration rate (GFR) and the amount of thrombocytes to ∼50% of basal values after 4 h.
View Article and Find Full Text PDFDecreased expression of a novel prostaglandin transporter, OAT-PG, facilitates renocortical PGE2 accumulation during rat pregnancy.
Gynecol Obstet Invest
July 2014
Department of Physiology I, Tohoku University Graduate School of Medicine, Sendai, Japan.
Background: Prostaglandin (PG)-specific organic anion transporter (OAT-PG) is a recently identified renal transporter involved in the local clearance of prostaglandin E2 (PGE2). Since the renal biosynthesis of PGE2 is not increased during pregnancy, this transporter expression would affect the gestational changes in the renal PGE2 content.
Methods: Kidneys from rats at different gestational stages were used to examine gestational changes in the renocortical PGE2 concentration.
Sex hormones induce a gender-related difference in renal expression of a novel prostaglandin transporter, OAT-PG, influencing basal PGE2 concentration.
Am J Physiol Renal Physiol
February 2012
Dept. of Molecular Physiology, College of Pharmaceutical Sciences, Kusatsu-City, Shiga, Japan.
Based on the nucleotide sequence of a mouse prostaglandin-specific transporter (mOAT-PG), we identified a rat homolog (rOAT-PG) which shares 80% identity with mOAT-PG in a deduced amino acid sequence. rOAT-PG transports PGE(2) and colocalizes with 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a metabolic enzyme for PGs, in proximal tubules, suggesting that rOAT-PG is involved in PGE(2) clearance to regulate its physiological function in the renal cortex. We found that the expression level of rOAT-PG in the renal cortex was much higher in male rats than in female rats whereas there was no gender difference in the expression level of cyclooxygenase-2, a key enzyme producing PGE(2), and 15-PGDH in the renal cortex.
View Article and Find Full Text PDFCOX-2 activity determines the level of renin expression but is dispensable for acute upregulation of renin expression in rat kidneys.
Am J Physiol Renal Physiol
June 2007
Institute für Pharmakologie, Universität Regensburg, Regensburg, Germany.
The role of cyclooxygenase 2 (COX-2) in the control of renin is still a matter of debate, since studies with COX-2-deficient mice or with COX-2 inhibitors produced conflicting findings. Therefore, we studied the effect of the COX-2 inhibitor SC-58236 on the regulation of the renin system in adult rat kidneys. Renocortical tissue levels and urinary excretion of PGE(2) were reduced to 65 and 40% of control values, respectively, after a single gavage of SC-58236 and did not further decrease on prolonged treatment.
View Article and Find Full Text PDFOntogeny and effects of thyroid hormone on beta1-adrenergic receptor mRNA expression in ovine fetal kidney cortex.
J Soc Gynecol Investig
December 2005
Department of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
Objective: Previous studies indicate that thyroidectomy (TX) decreases renin gene expression in ovine fetal renal cortex in late gestation. Fetal ovine renin-containing renocortical cells become increasingly responsive to beta-adrenergic stimulation as gestation proceeds. Increases in plasma thyroid hormone concentrations parallel this change, suggesting that there is a positive developmental relationship between the two.
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