title: Renal effects of hyperinsulinaemia in subjects with two hypertensive parents.
abstract: The aim of this investigation was to study the effects of isoglycaemic hyperinsulinaemia on the renal metabolism of electrolytes and water in subjects with a strong genetic predisposition to essential hypertension, compared with that in non-predisposed subjects. We studied 25 normotensive subjects aged 18-35 years whose parents both had essential hypertension, and 22 age- and sex-matched subjects whose parents were both normotensive. Diabetes or morbid obesity in any subject or parent excluded the family. The 24-h blood pressure was measured. The subjects received an isocaloric diet with a fixed content of sodium and potassium for 4 days before the study. An isoglycaemic, hyperinsulinaemic clamp with infusion of insulin (40 munits.min(-1).m(-2)) was performed. We measured the renal clearance of diethylenetriaminepenta-acetic acid, sodium, potassium and lithium both under basal conditions and during hyperinsulinaemia. In response to hyperinsulinaemia, renal sodium clearance decreased to a significantly greater extent in the hypertension-prone subjects [0.57 (0.74, 0.36) ml.min(-1).1.73 m(2) (median and quartiles)] than in the controls [0.34 (0.56, 0.18) ml. min(-1).1.73 m(2)] (P=0.04). Compared with the controls, the subjects predisposed to hypertension had a higher 24-h diastolic blood pressure [78 (70, 82) mmHg, compared with 73 (68, 77) mmHg], but a similar insulin sensitivity index ¿10(7)x[313 (225, 427)] compared with 10(7)x[354 (218, 435)] l(2).min(-1).pmol(-1).kg(-1)¿. Thus the sodium-retaining effect of insulin was more pronounced in subjects with a strong genetic predisposition to essential hypertension than in subjects with normotensive parents. This effect may contribute to the development of hypertension in subjects with a genetic predisposition to hypertension.
authors.affiliation: Department of Clinical Physiology, Hvidovre Hospital, DK-2650 Hvidovre, Denmark. uandersen@iname.com
authors.forename: U B
authors.initials: UB
authors.lastname: Andersen
authors.forename: P
authors.initials: P
authors.lastname: Skøtt
authors.forename: N E
authors.initials: NE
authors.lastname: Bruun
authors.forename: H
authors.initials: H
authors.lastname: Dige-Petersen
authors.forename: H
authors.initials: H
authors.lastname: Ibsen
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D006946:Hyperinsulinism / Q000378:metabolism*; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism; D007004:Hypoglycemic Agents; D007328:Insulin; D007668:Kidney / Q000378:metabolism*; D008094:Lithium / Q000493:pharmacokinetics; D008297:Male; D008657:Metabolic Clearance Rate; D010290:Parents; D004369:Pentetic Acid / Q000493:pharmacokinetics; D011188:Potassium / Q000493:pharmacokinetics; D012964:Sodium / Q000493:pharmacokinetics*; D018709:Statistics, Nonparametric
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D004369:Pentetic Acid; D008094:Lithium; D012964:Sodium; D011188:Potassium