Basal insulin-level oscillations in normotensive individuals with genetic predisposition to essential hypertension exhibit an irregular pattern.

BACKGROUND

Insulin is secreted in regular pulses at intervals of 12-14 min in normal fasting subjects. An abnormal pattern has been found in subjects with non-insulin-dependent diabetes mellitus (NIDDM) and in young individuals predisposed to NIDDM. It has been suggested that there might be a causal relationship between insulin-secretion abnormalities and insulin resistance.

OBJECTIVE

To examine whether insulin-secretion abnormalities are also present in offspring of patients with essential hypertension.

METHODS

Eleven young (aged 18-35 years) normotensive individuals each of whom had two parents with essential hypertension were compared with 10 age- and sex-matched controls each of whom had two normotensive parents. We verified that diabetes and morbid obesity were absent among the subjects and their parents. We studied basal insulin-secretion patterns during a 60 min period, glucose tolerance by administering an oral glucose-tolerance test, insulin resistance by using an isoglycaemic hyperinsulinaemic clamp and basal plasma catecholamine levels.

RESULTS

Autocorrelation analysis of insulin concentrations showed that the hypertension-prone subjects had a significantly reduced or irregular oscillatory pattern compared with the regular insulin-level oscillations with a period of 12-14 min in control subjects. The hypertension-prone subjects had significantly higher systolic blood pressures and tended to be insulin-resistant.

CONCLUSION

This is the first evidence of early insulin-secretion abnormalities in young normotensive individuals with a genetic predisposition to essential hypertension, but with a normal glucose tolerance and without a genetic predisposition to NIDDM. Early insulin-secretion abnormalities may be the very first step towards the development of insulin resistance and an important factor initiating the hypertension in hypertension-prone individuals.