Hyperinsulinemia and insulin resistance have been extensively reported in adult patients with essential hypertension. The aim of this study was to examine serum glucose and insulin levels both in the fasting state and after 0.25 g/kg IV glucose and to relate those findings to the status of intracellular Na + and red blood cell Na + -Li + countertransport in a population of 21 normolipemic normotensive offspring of hypertensive parents (N-EH) and 13 control children without a history of parental essential hypertension or diabetes mellitus matched for age, body mass index, and pubertal stage. Offspring of hypertensive parents presented significantly higher serum insulin levels both after an overnight fast (17.4±1.6 versus 11.6±1.6 fiU/mh in control [mean±SEM], P<.01) and after intravenous glucose than control subjects (insulin area under the curve, 3015±310 and 2057±234 jiU/mL per hour, respectively, P<.01). No relation could be established between the high red blood cell Na + -Li + countertransport (343±22 versus 215±15 /unol/L per hour, N-EH versus control; P<.002) or high intracellular Na + (9.8±0.28 versus 8.7 ±0.36 mEq/L, N-EH versus control) and hyperinsulinemia found in children of hypertensive parents. We conclude that the time precedence of hyperinsulinemia (and possibly insulin resistance) over the appearance of clinical hypertension in a high-risk population further supports the contention that an abnormal insulin action may play a pathogenetic role in essential hypertension. The lack of relation between hyperinsulinemia and red blood cell Na + -Li + countertransport or intracellular Na + suggests that either they are not linked in the causal pathway of hypertension or they are both an untimely product of a third yet undetermined pathogenetic factor.
Family history of hypertension and obesity are both risk factors for hypertension. Hypertension and obesity share several physiopathologic abnormalities and are frequently associated. However, not all obese people are hypertensive. Renal handling of sodium has been proposed as a physiopathogenic mechanism of essential hypertension and obesity. This study was conducted in obese adolescents to evaluate the role of a family history of hypertension versus obesity in the renal handling of sodium. .5% ؎ 1.3%, in ON it was 22.4% ؎ 2.3%, and in LH it was 14.4% ؎ 1.2% (P < .05). FEUA in OH was 8.5% ؎ 0.8%, in ON it was 14.8% ؎ 3.6%, and in LH it was 7.9% ؎ 0.8% (P < .01). Plasma renin activity (PRA) and aldosterone (PA) were measured in OH and LH; PRA was 5.3 ؎ 0.4 and 4.5 ؎ 0.4 ng/mL/h, respectively (P ؍ NS), and PA was 366 ؎ 36 and 242 ؎ 32 pg/mL, respectively (P < .05). In summary, adolescents with a family history of hypertension, regardless of their body mass, have a diminished FELi and FEUA. Obese adolescents also have higher plasma levels of aldosterone than lean ones. In conclusion, the family history of hypertension would be related to the increased renal proximal sodium reabsorption whereas obesity would be related to increased distal sodium reabsorption mechanisms, such as aldosterone. Both mechanisms could explain the higher prevalence of hypertension in obese offspring of hypertensive parents. Am J Hypertens 1999;12:260 -263
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 microU/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).(ABSTRACT TRUNCATED AT 250 WORDS)
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 (mumol 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 microU/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).(ABSTRACT TRUNCATED AT 250 WORDS)
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