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Journal of the American College of Nutrition, Vol 10, Issue 1 24-33, Copyright © 1991 by American College of Nutrition

JOURNAL ARTICLE

Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain

M. el Zein, J. L. Areas, J. Knapka, D. DiPette, B. Holland, P. al-Karadaghi and H. G. Preuss
Department of Medicine (Nephrology), Georgetown University Medical Center, Washington, D.C. 20007.

Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that "salt-sensitive" rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.




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Copyright © 1991 by the American College of Nutrition.