TY - JOUR
T1 - Experimentally induced acute hyperinsulinemia stimulates endogenous nitric oxide production in humans
T2 - Detection using urinary NO2-/NO3- excretion
AU - Tsukahara, Hirokazu
AU - Kikuchi, Kiyoshi
AU - Tsumura, Kumi
AU - Kimura, Kouki
AU - Hata, Ikue
AU - Hiraoka, Masahiro
AU - Sudo, Masakatsu
N1 - Funding Information:
From the Department of Pediatrics, Fukui Medical School, Fukui; and the Department of Pediatrics, Shimane Prefectural Central Hospital, lzumo, Japan. Submitted June 27, 1996; accepted September 6, 1996. Supported in part by a research grant from the Uehara Memorial Foundation. Address reprint requests to Hirokazu Tsukahara, MD, Department of Pediatrics, Fukui Medical School, Fukui 910-11, Japan. Copyright © !997 by W.B. Saunders Company 0026-0495/97/4604-0012503.00/0
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1997
Y1 - 1997
N2 - Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.
AB - Insulin-mediated glucose metabolism in skeletal muscle is associated with a proportional increase in muscle perfusion. The vasodilatory effect of insulin is thought to be mediated in part by endothelium-derived nitric oxide (NO). The present study was performed to determine whether acute hyperinsulinemia has any stimulatory effect on endogenous NO production in humans. Bolus intravenous injection of insulin (0.1 IU/kg body weight) caused a significant increase in urinary excretion of NO2-/NO3-together with s significant decrease in blood pressure, whereas saline infusion alone had no effect on these parameters. The increased NO response to insulin was almost comparable to that obtained with infusion of 30 g L-arginine. The acute effect of hyperinsulinemia on endogenous NO formation supports the concept that NO may mediate the vasodilatory action of insulin in humans.
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U2 - 10.1016/S0026-0495(97)90056-1
DO - 10.1016/S0026-0495(97)90056-1
M3 - Article
C2 - 9109844
AN - SCOPUS:0030901426
SN - 0026-0495
VL - 46
SP - 406
EP - 409
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 4
ER -
