From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Sun Aug 15 1999 - 06:03:17 MDT
Citations: 1-2
<1>
Authors
Yang BC. Li DY. Weng YF. Lynch J. Wingo CS. Mehta JL.
Institution
Department of Medicine, University of Florida and Veterans Affairs Medical
Center, Gainesville, Florida 32610, USA.
Title
Increased superoxide anion
generation and altered vasoreactivity in rabbits on low-potassium diet.
Source
American Journal of Physiology. 274(6 Pt 2):H1955-61, 1998 Jun.
Abstract
Potassium reduces blood pressure in populations at high risk of developing
hypertension, which suggests that potassium depletion may increase vascular
resistance. This study was designed to examine the effect of potassium
depletion on the L-arginine-nitric oxide pathway in arterial tissues. New
Zealand White rabbits were fed either a control diet, containing a normal
amount of potassium, or a low-potassium diet for 1-3 wk. As expected, the
low-potassium diet resulted in reduced serum and urinary potassium levels.
Carotid arteries were excised, and their contractile and relaxant responses
were determined in vitro. Carotid arterial ring contractile response to
norepinephrine was enhanced, and relaxation in response to the
endothelium-dependent vasodilators acetylcholine and calcium ionophore
A-23187 was attenuated, in rabbits fed low-potassium diet (all P < 0.01
compared with responses in rabbits fed control diet). The vasomotor responses
were similarly altered in rabbits fed low-potassium diet for 1 or 3 wk. Both
the enhanced contraction and attenuated relaxation were abolished by
treatment of arterial rings with superoxide dismutase but
not by treatment with L-arginine or indomethacin. Carotid artery rings from
rabbits fed the low-potassium diet showed approximately 100% greater
superoxide anion formation than those from
rabbits fed control diet (P < 0.01), whereas plasma and urinary nitrite
levels were similar in both groups of rabbits. These observations indicate
that low-potassium diet enhances the sensitivity of the carotid artery to
vasoconstrictor stimuli and reduces the sensitivity to endothelium-dependent
stimuli. Attenuation of endothelium-dependent relaxation appears to be
secondary to increased free radical generation, which may
degrade nitric oxide. Altered vasoreactivity may underlie the genesis of
hypertension in populations consuming diets low in potassium.
<2>
Authors
Jun T. Ke-yan F. Catalano M.
Institution
Research Center on Vascular Diseases, University of Milan, L. Sacco Hospital,
Italy.
Title
Increased superoxide anion
production in humans: a possible mechanism for the pathogenesis of
hypertension.
Source
Journal of Human Hypertension. 10(5):305-9, 1996 May.
Abstract
Although endothelium-dependent vasodilation is impaired in human
hypertension, the mechanism underlying this abnormality is not yet completely
elucidated. It has been suggested that accelerated inactivation of nitric
oxide (NO) due to superoxide anion, which
is rapidly removed by superoxide dismutase (SOD) in
physiological condition, may be related to hypertension. Therefore, SOD
deficiency following an increase in superoxide
anion production contributes to a rise in arterial blood
pressure (BP). We hypothesized that there is defective endogenous SOD in
patients with essential hypertension. To examine this assumption we measured
the SOD activities of the erythrocytes in 335 healthy Chinese volunteers (age
2-76 years) and 30 hypertensive patients (age 60-75 years). The SOD
activities of the healthy volunteers exhibited decreased trend with advancing
aging. There was no significant difference in the SOD activities between men
and women in each group. There is significant difference in the SOD
activities (1814.35 +/- 250.00 vs 1584.06 +/- 126.19 u/Hb.g; P < 0.001)
between the two groups (age 20-59 years; mean age 34 years vs age 60-76
years; mean age 67 years). The SOD activities in patients with essential
hypertension were 1322.4 +/- 139.5 u/Hb.g and significantly lower than the
corresponding healthy controls (P < 0.05). In the hypertensives, the SOD
activities against systolic and diastolic arterial pressure seem to be shown
the trend of negative correlation but did not reach the statistical
significance. We conclude that the SOD activities in the erythrocytes are
reduced in subjects with essential hypertension and increasing aging. The
present findings, in a limited data, could suggest that the fall in SOD
activities following an increased
superoxide anion production with
subsequently augmented NO inactivation is, at least in part, involved in the
pathogenesis of human hypertension, although the evidence is indirect. The
decrease in erythrocyte SOD activities may serve as a function of human
aging.
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