could NoSalt prevent hypertension from developing?

Doug Skrecky (
Sun, 15 Aug 1999 05:03:17 -0700 (PDT)

Citations: 1-2

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.


Jun T. Ke-yan F. Catalano M.
Research Center on Vascular Diseases, University of Milan, L. Sacco Hospital, Italy.
Increased superoxide anion
production in humans: a possible mechanism for the pathogenesis of hypertension.
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.