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.

Increased superoxide anion production in humans: a possible mechanism for the pathogenesis of hypertension / T. Jun, F. Ke-yan, M. Catalano. - In: JOURNAL OF HUMAN HYPERTENSION. - ISSN 0950-9240. - 10:5(1996), pp. 305-309.

Increased superoxide anion production in humans: a possible mechanism for the pathogenesis of hypertension

M. Catalano
Ultimo
1996

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.
Aging; Nitric oxide; Superoxide anion; Superoxide dismutase
Settore MED/09 - Medicina Interna
1996
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/157765
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