RESUMO
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. Fractional excretion of lithium (FELi) and uric acid (FEUA) were measured in 46 obese adolescent offspring of hypertensive parents (OH: body mass index [BMI], 29.5 +/- 0.6 kg/m2, age 14.2 +/- 0.3 years, 22 males); eight obese offspring of normotensive parents (ON: BMI, 30.7 +/- 1.7 kg/m2, 14.8 +/- 0.8 years, four males), and in 34 lean adolescent offspring of hypertensive parents (LH: BMI, 20.5 +/- 0.5 kg/m2, 14.3 +/- 0.3 years, 24 males). FELi in OH was 16.5% +/- 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.
Assuntos
Hipertensão/genética , Obesidade/genética , Adolescente , Índice de Massa Corporal , Hemodinâmica , Humanos , Hipertensão/etiologia , Hipertensão/fisiopatologia , Masculino , Obesidade/fisiopatologia , Sistema Renina-Angiotensina/fisiologia , Fatores de RiscoRESUMO
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)
Assuntos
Adolescente , ATPases Transportadoras de Cálcio/sangue , Filho de Pais com Deficiência , Eritrócitos/enzimologia , Hipertensão/genética , Insulina/sangue , Adulto , Cálcio/urina , Criança , Colesterol/sangue , Interpretação Estatística de Dados , Feminino , Teste de Tolerância a Glucose , Humanos , Masculino , Radioimunoensaio , Espectrofotometria AtômicaRESUMO
Creatinine clearance and microalbuminuria were measured before and after an oral protein load in 17 children with a history of haemolytic uraemic syndrome, 11 with a single kidney, and 15 controls, all of them normotensive and without evidence of renal damage, to look for indirect evidence of glomerular hyperfiltration. While creatinine clearance increased significantly after the protein load in controls, it did not change in patients with either haemolytic uraemic syndrome or a single kidney. Basal microalbuminuria was significantly higher in those with haemolytic uraemic syndrome when compared with those with a single kidney and controls. It increased significantly in all groups after a water load; this increase was significantly higher in haemolytic uraemic syndrome. After the protein load microalbuminuria returned to baseline. In conclusion, children with a history of haemolytic uraemic syndrome have an abnormal renal functional reserve like children with a single kidney. Only patients with haemolytic uraemic syndrome exhibited an increased microalbuminuria, however, suggesting that it may be the expression of a pathophysiological mechanism involved in haemolytic uraemic syndrome and not in single kidney, that could account for their different prognosis.