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Insulin regulates nitric oxide production in the kidney collecting duct cells.
Pandey, Gaurav; Makhija, Ekta; George, Nelson; Chakravarti, Bandana; Godbole, Madan M; Ecelbarger, Carolyn M; Tiwari, Swasti.
Afiliación
  • Pandey G; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and.
  • Makhija E; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and.
  • George N; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and.
  • Chakravarti B; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and.
  • Godbole MM; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and.
  • Ecelbarger CM; the Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, D. C. 2007.
  • Tiwari S; From the Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and tiwaris@sgpgi.ac.in.
J Biol Chem ; 290(9): 5582-91, 2015 Feb 27.
Article en En | MEDLINE | ID: mdl-25533472
The kidney is an important organ for arterial blood pressure (BP) maintenance. Reduced NO generation in the kidney is associated with hypertension in insulin resistance. NO is a critical regulator of vascular tone; however, whether insulin regulates NO production in the renal inner medullary collecting duct (IMCD), the segment with the greatest enzymatic activity for NO production in kidney, is not clear. Using an NO-sensitive 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM) fluorescent dye, we found that insulin increased NO production in mouse IMCD cells (mIMCD) in a time- and dose-dependent manner. A concomitant dose-dependent increase in the NO metabolite (NOx) was also observed in the medium from insulin-stimulated cells. NO production peaked in mIMCD cells at a dose of 100 nm insulin with simultaneously increased NOx levels in the medium. At this dose, insulin significantly increased p-eNOS(Ser1177) levels in mIMCD cells. Pretreatment of cells with a PI 3-kinase inhibitor or insulin receptor silencing with RNA interference abolished these effects of insulin, whereas insulin-like growth factor-1 receptor (IGF-1R) silencing had no effect. We also showed that chronic insulin infusion to normal C57BL/6J mice resulted in increased endothelial NOS (eNOS) protein levels and NO production in the inner medulla. However, insulin-infused IRKO mice, with targeted deletion of insulin receptor from tubule epithelial cells of the kidney, had ∼50% reduced eNOS protein levels in their inner medulla along with a significant rise in BP relative to WT littermates. We have previously reported increased baseline BP and reduced urine NOx in IRKO mice. Thus, reduced insulin receptor signaling in IMCD could contribute to hypertension in the insulin-resistant state.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Insulina / Médula Renal / Túbulos Renales Colectores / Óxido Nítrico Límite: Animals Idioma: En Revista: J Biol Chem Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Insulina / Médula Renal / Túbulos Renales Colectores / Óxido Nítrico Límite: Animals Idioma: En Revista: J Biol Chem Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos