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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ontogenic expression of mRNAs encoding the V1a and V2 vasopressin receptors (V1aR and V2R) was visualized in liver and kidney of embryonic, developing, and adult rats using in situ hybridization histochemistry. Transcripts were detected at 16 and 19 days gestational age in kidney, with V1aR mRNA predominating in the developing cortex and V2R in the medulla. V1aR transcripts in 1-day-old kidneys were in vascular elements, in cells of developing medullary collecting ducts, and over mesangial cells of deep glomeruli, consistent with a role for the V1aR in regulating cellular growth. Expression of V1aR mRNA in the adult was found mainly in medullary vascular elements, arcuate and interlobular arteries, short segments of the cortical distal tubule, and transitional epithelium and smooth muscle of the pelvic wall and ureter. V2R mRNA, at 16 and 19 days gestational age, was in cells of developing medullary and cortical collecting ducts and, after birth, in cells of differentiating thick limbs of the loops of Henle, papillary surface epithelium, overlying macula densa, and short distal nephron segments. This distribution is in accord with the known role of V2 receptors in regulating water excretion. In contrast to kidney, liver did not express V2R mRNA and expressed V1aR transcripts only after birth. V1aR mRNA labeling was over cells bordering central veins on day 1 and surrounding central veins by day 5. A gradient was maximal on postnatal day 21, with V1aR mRNA most abundant in hepatocytes surrounding central veins and virtually absent in periportal hepatocytes. By day 60, most hepatocytes expressed V1aR transcripts, and the gradient was reduced. The ontogenic expression and receptor mRNA gradient are consistent with a role for hepatic V1a receptors in glucoregulation. These experiments confirm the presence of both V1a and V2 receptors in kidney and show that vasopressin receptor mRNA expression is developmentally regulated and tissue specific.
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PMID:Expression of vasopressin V1a and V2 receptor messenger ribonucleic acid in the liver and kidney of embryonic, developing, and adult rats. 840 28

Congenital nephrogenic diabetes insipidus (NDI) is a chronic disorder involving polyuria and polydipsia that results from unresponsiveness of the renal collecting ducts to the antidiuretic hormone vasopressin. Either of the genetic defects in vasopressin V2 receptor or the water channel aquaporin 2 (AQP2) cause the disease, which interfere the water reabsorption at the epithelium of the collecting duct. An unconscious state including a perioperative situation can be life threatening because of the difficulty to regulate their water balance. The Sendai virus (SeV) vector system deleting fusion protein (F) gene (SeV/DeltaF) is considered most suitable because of the short replication cycle and nontransmissible character. An animal model for NDI with reduced AQP2 by lithium chloride was used to develop the therapy. When the SeV/DeltaF vector carrying a human AQP2 gene (AQP2-SeV/DeltaF) was administered retrogradely via ureter to renal pelvis, AQP2 was expressed in the renal collecting duct to reduce urine output and water intake by up to 40%. In combination with the retorograde administration to pelvis, this system could be the cornerstone for the applicable therapies on not only NDI patients but also other diseases associate with the medullary collecting duct.
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PMID:Novel treatment for lithium-induced nephrogenic diabetes insipidus rat model using the Sendai-virus vector carrying aquaporin 2 gene. 1865 13