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1 Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia, Australia
2 Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia, Australia; Department of Geriatric Medicine, The Queen Elizabeth Hospital, Adelaide, South Australia, Australia
3 Department of Clinical Pharmacology, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia, Australia
* To whom correspondence should be addressed. E-mail: karen.jones{at}adelaide.edu.au.
The primary aims of this study were to evaluate the effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine-methyl-ester (L-NAME), on gastric emptying (GE) of, and the blood pressure (BP), glycemic, insulin and incretin responses to, oral glucose in older subjects. Eight healthy subjects (4 male and 4 female, aged 70.9 ± 1.3 years) were studied on two separate days, in double-blind, randomized order. Subjects received an intravenous (I.V.) infusion of either L-NAME (180µg/kg/hr) or saline (0.9%) at a rate of 3ml/min for 150 minutes. Thirty minutes after the commencement of the infusion (t = 0 minutes), subjects consumed a 300ml drink containing 50g glucose labeled with 20MBq 99mTc-sulfur colloid, while sitting in front of a gamma camera. GE, BP (systolic and diastolic), heart rate (HR), blood glucose, plasma insulin and incretin hormones, glucose-dependant insulinotropicpolypeptide (GIP) and glucagon-like peptide 1 (GLP-1), were measured. L-NAME had no effect on GE, GIP and GLP-1. Between t = -30 - 0 minutes L-NAME had no effect on BP or HR. After the drink (t = 0 - 60 minutes) systolic and diastolic BP fell (P<0.05) and HR increased (P<0.01) during saline; these effects were attenuated (P<0.001) by L-NAME. Blood glucose levels between 90 - 150 minutes were higher (P<0.001) and plasma insulin between 15 - 150 minutes less (P<0.001) after L-NAME. The fall in BP, increase in HR and stimulation of insulin secretion by oral glucose in older subjects are mediated by NO mechanisms by an effect unrelated to GE or changes in incretin hormones.
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