(Hypertension. 2000;36:423.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Enhanced NO Inactivation and Hypertension Induced by a High-Fat, Refined-Carbohydrate Diet
From the Department of Physiological Science (C.K.R., R.J.B.), University of California, Los Angeles, and the Division of Nephrology and Hypertension (N.D.V., X.Q.W.), Department of Medicine, University of California, Irvine.
Correspondence to R. James Barnard, PhD, Department of Physiological Science, UCLA, PO Box 951527, Los Angeles, CA 90095-1527. E-mail jbarnard{at}ucla.edu
Abstract—We have recently
demonstrated that long-term consumption of a high-fat,
refined-carbohydrate (HFS) diet induces hypertension (HTN) in normal
rats compared with a low-fat, complex-carbohydrate (LFCC) diet. Limited
evidence suggests that high-fat or high-sugar diets cause enhanced
generation of reactive oxygen species (ROS). We therefore hypothesized
that by inducing oxidative stress, the HFS diet may promote nitric
oxide (NO) inactivation and HTN. To test this hypothesis, female
Fischer rats were placed on either the HFS or the LFCC diet starting at
2 months of age. Blood pressure, urinary NO metabolites
(NOx), and total renal NO synthase activity were
monitored, and the tissue abundance of nitrotyrosine (NT), which is the
stable "footprint" of NO oxidation by ROS, was determined. The HFS
diet group exhibited a gradual rise in arterial blood
pressure and were hypertensive by 18 months. This trend was accompanied
by a marked accumulation of NT in all tested tissues, an initial rise
and a subsequent fall in NO synthase activity, and a fall in urinary
NOx excretion. The HFS diet–fed animals had a
blunted blood pressure response to the NO synthase
inhibitor
N
-nitro-L-arginine
methyl ester (L-NAME) compared with the LFCC diet
group, which showed a marked hypertensive response to
L-NAME. L-NAME–induced HTN
was reversible with L-arginine in the LFCC diet
group; however, HTN was not corrected by
L-arginine supplementation in the HFS diet group.
These findings point to enhanced ROS-mediated inactivation and
sequestration of NO, which may contribute to the reduction of bioactive
NO and HTN in the HFS diet–fed animals.
Key Words: arginine • endothelial • free radicals • insulin resistance • L-NAME • nitric oxide
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