The common association between diabetes mellitus and hypertension may be promoted by several mechanisms. Patients with insulin-dependent (type I) diabetes and prone to develop nephropathy often have a familial predisposition for essential hypertension, whereas normotensive healthy offspring of nondiabetic essential hypertensive parents tend to have a reduced insulin sensitivity and increased plasma insulin levels. Na+ retention occurs as a characteristic alteration in type I or non-insulin-dependent (type II) diabetes; exchangeable body Na+ (Naex) is increased by 10% on average. This abnormality develops in the uncomplicated stage of diabetes and differentiates diabetic from nondiabetic essential hypertensive subjects. Possible Na(+)- retaining mechanisms include increased glomerular filtration of glucose leading to enhanced proximal tubular Na(+)-glucose cotransport, hyperinsulinemia (which activates several tubular Na+ transporters), an extravascular shift of fluid with Na+, and, once it occurs, renal failure. The pathogenetic role of Na+ retention in diabetes-associated hypertension is supported by positive correlations between systolic or mean blood pressure and Naex and by normalization of blood pressure after removal of excess Na+ by diuretic treatment in hypertensive diabetic subjects. The latter may also have an enhanced sensitivity of blood pressure to Na+. Plasma levels of active renin, angiotensin II, aldosterone, and catecholamines are usually normal or low in metabolically stable type I or type II diabetes. However, an exaggerated vascular reactivity to norepinephrine and angiotensin II commonly occurs already at uncomplicated stages of type I or type II diabetes. This may be a manifestation of functional (i.e., intracellular electrolytes) and/or morphological (proliferation, narrowing, and stiffening) vasculopathy. Diabetes-associated Na+ retention, vasculopathy, and a presumably inherited predisposition for both diabetes and essential hypertension may represent important complementary factors favoring the frequent occurrence of hypertension in the diabetic population.
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Original Articles|
March 01 1991
Central Role of Sodium in Hypertension in Diabetic Subjects
Peter Weidmann, MD;
Peter Weidmann, MD
Medizinische Poliklinik, University of Berne
Berne, Switzerland
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Paolo Ferrari, MD
Paolo Ferrari, MD
Medizinische Poliklinik, University of Berne
Berne, Switzerland
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Address correspondence and reprint requests to Peter Weidmann, MD, Professor of Medicine, Medizinische Poliklinik, University of Berne, Freiburgstrasse 3, CH-3010, Bern, Switzerland.
Citation
Peter Weidmann, Paolo Ferrari; Central Role of Sodium in Hypertension in Diabetic Subjects. Diabetes Care 1 March 1991; 14 (3): 220–232. https://doi.org/10.2337/diacare.14.3.220
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