Glucose scavenging of nitric oxide

• DOI: 10.1152/ajprenal.2001.280.3.f480
• Publication Date: 2017-12-23T08:15:32Z
• Authors: Sergey V. Brodsky; Albert Marcus Mor...; Nimish Dharia; Steven S. Gross; Michael S. Goligo...
• Keywords: Endothelial Dysfunction; Nitrotyrosine

Endothelial dysfunction accompanies suboptimal glucose control in patients with diabetes mellitus. A hallmark of endothelial is a deficiency production or bioavailability vascular nitric oxide (NO). Here we demonstrate that acute exposure human cells to glucose, at levels found plasma diabetic patients, results significant blunting NO responses the synthase (eNOS) agonists bradykinin and A-23187. Monitoring generation by purified recombinant bovine eNOS vitro, using amperometric electrochemical detection an NO-selective porphyrinic microelectrode, showed causes progressive concentration-dependent attenuation detectable NO. Addition pure solutions similarly elicited sharp decrease concentration, indicating promotes loss. Electrospray ionization-tandem mass spectrometry, negative ion monitoring, directly demonstrated occurrence covalent reaction involving unitary addition (or derived species) glucose. Collectively, our findings reveal hyperglycemia chemical inactivation NO; this glucose-mediated loss may contribute hypertension patients.