(Hypertension. 1995;26:1089-1092.)
© 1995 American Heart Association, Inc.
Articles |
From the Hypertension Clinic, Hospital de Niños "Ricardo Gutierrez," Buenos Aires, Argentina.
Correspondence to Beatriz Grunfeld, La Pampa 3635, Buenos Aires 1430, Argentina.
Abstract We previously showed that children and adolescent offspring of patients with essential hypertension have an increased proximal renal sodium reabsorption as measured by lithium fractional excretion. Insulin has been shown to have antinatriuretic properties and to be increased (hyperinsulinemia) in essential hypertension. The aim of this study was to evaluate the role of insulin on the increased proximal renal sodium reabsorption previously reported. Lithium and sodium fractional excretions were measured 3 hours before and 3 hours after an intravenous glucose tolerance test in 20 normotensive adolescents with a family history of essential hypertension (F+, 14.8±0.5 years) and 10 normotensive control subjects without a family history of hypertension (F-, 15.2±0.9 years). Results are mean±SEM. Lithium fractional excretion before glucose loading was 16.1±1.8% in F+ versus 23.5±2.0% in F- (P<.02) and after glucose loading was 14.7±1.3% in F+ versus 20.9±1.7% in F- (P=NS). Lithium fractional excretion did not change after intravenous glucose loading in either group. The insulin area under the curve was 2815±499 in F+ versus 2290±418 µU/mL per hour in F- (P=NS). There was no correlation between lithium fractional excretion and insulin area under the curve. Fractional excretion of sodium before glucose loading was 0.99±0.1% in F+ versus 0.99±0.1% in F- (P=NS) and after glucose loading was 0.77±0.1 in F+ versus 0.85+0.1% in F- (P<.01 versus values before loading in both groups). In summary lithium fractional excretion did not change after the intravenous glucose loading, and no correlation was found with insulin levels. Thus, insulin does not appear to be involved in the decreased lithium fractional excretion in F+. However, sodium fractional excretion diminished significantly after the intravenous glucose loading. Therefore, our findings in physiological conditions in humans show that one possible role of insulin in the development of hypertension is through an antinatriuretic effect distal to the proximal tubule.
Key Words: insulin hypertension, genetic sodium
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