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Possible Involvement of Anorexigenic Protein, Nesfatin/Nucleobindin-2 (NUCB2) in Blood Pressure Regulation by Regulating Water Reabsorption in Renal Collecting Duct

Abstract

Hiroyuki Shimizu and Aya Osaki

Nesfatin/nucleobindin-2 (NUCB2), a precursor protein of anorexigenic protein, nesfatin-1, is ubiquitously expressed in the body. The finding that peripheral administration of nesfatin-1 increases blood pressure indicates a possible involvement of nesfatin-1 in the regulation of blood pressure. The present studies were undertaken to investigate a possible involvement of nesfatin/NUCB2 in the regulation of blood pressure. The immunoreactivity against nesfatin/NUCB2 was selectively found in vascular endothelial cells of aorta, pulmonary artery and renal artery, cardiac muscle and skeletal striated muscle cells, but not in vascular smooth muscle cells at all. Furthermore, the immunoreactivity against nesfatin/NUCB2 was selectively found in renal collecting duct cells, which contain aquaporin (AQP)-2 and/or epithelial sodium channel (ENaC). In medullary collecting ducts, cells expressing nesfatin/ NUCB2 co-expressed AQP-2, but did not co-expressed AQP-2 in renal cortical collecting ducts. On the other hand, collecting ductal cells expressing ENaC were totally compatible with those expressing nesfatin/NUCB2 in both renal medullary and cortical collecting ducts. Thus, there is a possibility that nesfatin/NUCB2 is involved in the regulation of blood pressure through increased water reabsorption in the kidney.

Avertissement: Ce résumé a été traduit à l'aide d'outils d'intelligence artificielle et n'a pas encore été examiné ni vérifié

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