( 1987) demonstrated an augmented insulin response to oral glucose, as well as fasting hyperlipidemia, in hypertensives. Shen et al. ( 1988) studied lean Chinese males with the insulin suppression test, and found blunted glucose disposal in hypertensives. In a rigorous experimental study, Ferrannini et al. ( 1987) utilized a euglycemic hyperinsulinemic clamp technique to study insulin resistance in lean, hypertensive adults with normal glucose tolerance. Compared to age- and weight-matched normotensive controls, the hypertensives exhibited marked impairment of glucose uptake in response to the insulin infusion. Their data provide substantial evidence that EH is associated with insulin resistance independent of obesity or carbohydrate intolerance in middle-aged adults. Zavaroni et al. ( 1989) demonstrated, in a population of 247 lean subjects with normal glucose tolerance, that fasting insulin concentration greater than 2 SD above the mean predicted hypertriglyceridemia as well as elevated blood pressure. They also found that augmented insulin response during oral glucose tolerance testing in this group was correlated with elevated blood pressure. They concluded that hyperinsulinemia in the absence of impaired glucose tolerance predicts elevated blood pressure. The sum of evidence from these studies is that insulin resistance is a determinant of blood pressure in adults and may also be engaged in the pathogenesis of EH.
An alteration in sympathetic nervous system activity may also be involved in insulin resistance. Chronic insulin release has been shown to be stimulated by beta-mediated sympathetic activity (which is regarded to be higher in EH). It had been suggested that the peripheral uptake of glucose would decrease with increasing beta-receptor mediated sympathetic activity, resulting in decreased insulin sensitivity ( Berglund et al., 1976). However, more recently Rowe et al. ( 1981) utilized the hyperinsulinemic euglycemic clamp technique to demonstrate a significant increase in plasma norepinephrine levels in response to euglycemic hyperinsulinemia. Cardiovascular measurements demonstrated a concurrent increase in blood pressure. This study indicates that elevated levels of plasma insulin may increase sympathetic nervous system activity in the absence of changes in blood glucose.
Fasting suppresses sympathetic nervous system activity and refeeding stimulates sympathetic nervous system activity ( O'Hare, 1988). The interrelationship of carbohydrate intake, insulin resistance, and sympathetic nervous system activity remains to be clarified. However, there is presently evidence that supports a role of this adrenergic-metabolic interaction at an early phase in the pathogenesis of hypertension and cardiovascular disease.
Anderson N. B., Lane J. D., Muranka M., Williams R. B., & Houseworth S. J. ( 1988). "Racial differences in blood pressure and forearm vascular responses to the cold face stimulus". Psychosomatic Medicine, 50, 57-63.