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Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice

Chennupati, Ramesh ; Meens, Merlijn J. ; Janssen, Ben J. ; Dijk, Paul ; Hakvoort, Theodorus B. M. ; Lamers, Wouter H. ; De Mey, Jo G. R. ; Koehler, S. Eleonore

Physiological reports, 2018-06, Vol.6 (11), p.e13717-n/a [Periódico revisado por pares]

United States: John Wiley & Sons, Inc

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Título:
Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice
Autor: Chennupati, Ramesh ; Meens, Merlijn J. ; Janssen, Ben J. ; Dijk, Paul ; Hakvoort, Theodorus B. M. ; Lamers, Wouter H. ; De Mey, Jo G. R. ; Koehler, S. Eleonore
Assuntos: Acetylcholine ; Animals ; Arginase ; Arginase - genetics ; Arginase - metabolism ; Arginase 1 deficiency ; Arginine ; Arterial Pressure ; Arteries ; Arteries - physiopathology ; Blood pressure ; Cardiovascular Conditions, Disorders and Treatments ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus - metabolism ; Diabetes Mellitus - physiopathology ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - physiopathology ; Disease Models, Animal ; Endocrine and Metabolic Conditons, Disorders and Treatments ; Endothelial Cells - metabolism ; endothelial dysfunction ; Endothelium ; Hemodynamics ; Hyperglycemia ; Hyperpolarization ; Immunohistochemistry ; Intravenous administration ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle contraction ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric-oxide synthase ; Original Research ; Phenylephrine ; Physiology ; Rodents ; Signalling Pathways ; Smooth Muscle ; Sodium ; Sodium nitroprusside ; Streptozocin ; Vasodilation
É parte de: Physiological reports, 2018-06, Vol.6 (11), p.e13717-n/a
Notas: This work was supported by the grant from Dutch Heart Foundation (NHS) project 2008B107.
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Descrição: Endothelial arginase 1 was ablated to assess whether this prevents hyperglycemia‐induced endothelial dysfunction by improving arginine availability for nitric oxide production. Endothelial Arg1‐deficient mice (Arg1‐KOTie2) were generated by crossing Arg1fl/fl (controls) with Tie2Cretg/− mice and analyzed by immunohistochemistry, measurements of hemodynamics, and wire myography. Ablation was confirmed by immunohistochemistry. Mean arterial blood pressure was similar in conscious male control and Arg1‐KOTie2 mice. Depletion of circulating arginine by intravenous infusion of arginase 1 or inhibition of nitric oxide synthase activity with L‐NG‐nitro‐arginine methyl ester increased mean arterial pressure similarly in control (9 ± 2 and 34 ± 2 mmHg, respectively) and Arg1‐KOTie2 mice (11 ± 3 and 38 ± 4 mmHg, respectively). Vasomotor responses were studied in isolated saphenous arteries of 12‐ and 34‐week‐old Arg1‐KOTie2 and control animals by wire myography. Diabetes was induced in 10‐week‐old control and Arg1‐KOTie2 mice with streptozotocin, and vasomotor responses were studied 10 weeks later. Optimal arterial diameter, contractile responses to phenylephrine, and relaxing responses to acetylcholine and sodium nitroprusside were similar in normoglycemic control and Arg1‐KOTie2 mice. The relaxing response to acetylcholine was dependent on the availability of extracellular l‐arginine. In the diabetic mice, arterial relaxation responses to endothelium‐dependent hyperpolarization and to exogenous nitric oxide were impaired. The data show that endothelial ablation of arginase 1 in mice does not markedly modify smooth muscle and endothelial functions of a resistance artery under normo‐ and hyperglycemic conditions. Arginases share the substrate arginine with nitric oxide synthase and may, thus, modulate nitric oxide production. We report that severe depletion of circulating arginine disturbs vasomotor responses, whereas ablation of endothelial arginase 1 has no beneficial effect.
Editor: United States: John Wiley & Sons, Inc
Idioma: Inglês

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Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice

Chennupati, Ramesh ; Meens, Merlijn J. ; Janssen, Ben J. ; Dijk, Paul ; Hakvoort, Theodorus B. M. ; Lamers, Wouter H. ; De Mey, Jo G. R. ; Koehler, S. Eleonore

United States: John Wiley & Sons, Inc

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