| Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia. | |
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MedLine Citation:
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PMID: 9107164 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Acute hyperglycemia may increase vascular tone in normal humans via a glutathione-sensitive, presumably free radical-mediated pathway. The objective of this study was to investigate whether or not the vascular effects of hyperglycemia are related to reduced availability of nitric oxide. METHODS AND RESULTS: Acute hyperglycemia (15 mmol/L, 270 mg/dL) was induced in 12 healthy subjects with an artificial pancreas. Systolic and diastolic blood pressures, heart rate, and plasma catecholamines showed significant increases (P < .05) starting after 30 minutes of hyperglycemia; leg blood flow decreased significantly (15%; P < .05) at 60 and 90 minutes. Platelet aggregation to ADP and blood viscosity also showed significant increments (P < .05). The infusion of L-arginine (n = 7, 1 g/min) but not D-arginine (n = 5, 1 g/min) or L-lysine (n = 5, 1 g/min) in the last 30 minutes of the hyperglycemic clamp completely reversed all hemodynamic and rheological changes brought about by hyperglycemia. Infusion of NG-monomethyl-L-arginine (L-NMMA; 2 mg/min) to inhibit endogenous nitric oxide synthesis in 8 normal subjects produced vascular effects qualitatively similar to those of hyperglycemia but quantitatively higher (P < .05); however, heart rate and plasma catecholamine levels decreased during L-NMMA infusion, presumably as a consequence of baroreflex activation. Infusion of L-NMMA during hyperglycemia produced changes not different from those obtained during infusion of L-NMMA alone. CONCLUSIONS: The results show that acute hyperglycemia in normal subjects causes significant hemodynamic and rheological changes that are reversed by L-arginine. Moreover, the effects of hyperglycemia are mimicked to a large extent, but not entirely, by infusion of L-NMMA. This suggests that hyperglycemia may reduce nitric oxide availability in humans. |
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Authors:
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D Giugliano; R Marfella; L Coppola; G Verrazzo; R Acampora; R Giunta; F Nappo; C Lucarelli; F D'Onofrio |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Circulation Volume: 95 ISSN: 0009-7322 ISO Abbreviation: Circulation Publication Date: 1997 Apr |
Date Detail:
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Created Date: 1997-05-13 Completed Date: 1997-05-13 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1783-90 Citation Subset: AIM; IM |
Affiliation:
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Department of Geriatrics and Metabolic Diseases, Second University of Naples, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Adult Arginine / pharmacology* Blood Viscosity / drug effects Catecholamines / blood Female Free Radicals Glucose / diagnostic use Glutathione / physiology Hemodynamics / drug effects Humans Hyperglycemia / physiopathology* Insulin / blood Lysine / pharmacology Male Nitric Oxide / biosynthesis, physiology* Platelet Aggregation / drug effects Vasoconstriction / drug effects* omega-N-Methylarginine / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Catecholamines; 0/Free Radicals; 10102-43-9/Nitric Oxide; 11061-68-0/Insulin; 17035-90-4/omega-N-Methylarginine; 50-99-7/Glucose; 56-87-1/Lysine; 70-18-8/Glutathione; 74-79-3/Arginine |
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