CALCIUM-ATPASE AND INSULIN IN ADOLESCENT OFFSPRING OF ESSENTIAL HYPERTENSIVE PARENTS

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 Ca2+-ATPase. We have previously show n that normotensive offspring of essential hypertensive individuals ha ve an exaggerated insulin response to a glucose overload. Therefore, t he aim of the present study was to evaluate basal and calmodulin-activ ated Ca2+-ATPase in red blood cells and its relationship to the insuli n response during an intravenous glucose tolerance rest in 27 normoten sive adolescents with a family history of essential hypertension (F+) (mean age, 13.9+/-0.5 years) and in 10 control subjects matched for ag e and body mass index with no family history of hypertension (F-). The results (mean+/-SD) were as follows (mu mol Pi/[mg protein/h]10(-1)): basal Ca2+ ATPase, 4.5+/-1.2 in F+ and 5.1+/-1.6 in F- (P=NS); calmod ulin-activated Ca2+-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 mu U/mL per hour in F+ and 2752+/-928 in F- (P=NS). Calmodulin- activated Ca2+-ATPase showed a negative correlation with the insulin a rea 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 Ca2+-ATPase despite increased levels of insu lin, a known activator of this pump, further suggesting the presence o f insulin resistance in normotensive offspring of essential hypertensi ve individuals. Since Ca2+-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.