Calcium-ATPase and Insulin in Adolescent Offspring of Essential Hypertensive Parents

Abstract

Abstract A number of abnormalities in calcium homeostasis have been reported in patients with essential hypertension. In turn, insulin has been shown to influence the activity of the Ca 2+ -ATPase. We have previously shown that normotensive offspring of essential hypertensive individuals have an exaggerated insulin response to a glucose overload. Therefore, the aim of the present study was to evaluate basal and calmodulin-activated Ca 2+ -ATPase in red blood cells and its relationship to the insulin response during an intravenous glucose tolerance test in 27 normotensive adolescents with a family history of essential hypertension (F+) (mean age, 13.9±0.5 years) and in 10 control subjects matched for age and body mass index with no family history of hypertension (F−). The results (mean±SD) were as follows (μmol Pi/[mg protein/h]10 −1 ): basal Ca 2+ -ATPase, 4.5±1.2 in F+ and 5.1±1.6 in F− ( P =NS); calmodulin-activated Ca 2+ -ATPase, 13.6±3.9 in F+ and 16.2±1.7 in F− ( P <.04). The insulin area under the curve after the glucose load was 3413±1674 μU/mL per hour in F+ and 2752±928 in F− ( P =NS). Calmodulin-activated Ca 2+ -ATPase showed a negative correlation with the insulin area under the curve ( r =−.59, P <.005) and cholesterol levels ( r =−.38, P <.03). Urinary calcium excretion was 1.82±0.9 mmol/d in F+ and 2.47±0.9 mmol/d in F− ( P =NS). Our findings indicate a diminished activity of calmodulin-stimulated Ca 2+ -ATPase despite increased levels of insulin, a known activator of this pump, further suggesting the presence of insulin resistance in normotensive offspring of essential hypertensive individuals. Since Ca 2+ -ATPase is an extrusion pump, a drop in its activity may lead to an increase in intracellular calcium accumulation and thus contribute to the development of hypertension.