[Hyperinsulinism/insulin resistance: cause, effect or marker of essential arterial hypertension?]

Essential hypertension is often accompanied by metabolic abnormalities which commonly include hyperinsulinemia/insulin resistance. Even in the absence of these metabolic disorders, high blood pressure tends to be associated with insulin resistance. These observations raise two orders of questions: 1) whether hyperinsulinemia and insulin resistance are simply innocent bystanders or are causally involved in the initiation and/or promotion of hypertension; 2) whether blood pressure elevation is eventually caused by excess of insulin or whether it is a manifestation of the complex metabolic state responsible for insulin resistance. The purpose of this paper is to survey the clinical, epidemiological and experimental data that have led to the above generalizations and to address the potential significance of this coexistence. First, it could be argued that the relationship between high blood pressure and the associated metabolic defects is incidental. In this case, insulin resistance and hypertension may represent two independent consequences of a same metabolic disorder. On the other hand, there is evidence that suggests that insulin resistance (by itself or by insulin) may play a role in the etiology and/or the clinical course of hypertension. Although insulin has complex actions on the circulation (including a vasodilator effect), plausible mechanisms by which insulin might raise blood pressure include stimulation of the sympathetic nervous system, alteration of ion transport kinetics, increase of renal sodium retention and stimulation of vascular smooth cells growth. The pathways that could link insulin resistance, through hyperinsulinemia, with essential hypertension are based on the concept that a defect of insulin action on glucose utilization, does not imply that all other effects of insulin are equally blunted. However, in patients with insulinoma, hypertension has not been associated, and the acute administration of insulin does not cause an increase in blood pressure. It is also possible, on the contrary, that hypertension may be the cause of insulin resistance, but in various forms of secondary hypertension, impaired insulin sensitivity has not been found. It is probable that insulin resistance may represent, in a subgroup of individuals characterized by genetic predisposition (ethnicity, familiarity, etc.), simply a marker for susceptibility to hypertension. Hyperinsulinemia, in these subjects, may directly contribute to a raise in blood pressure by several mechanisms. In conclusion, despite the clinical importance of this association the nature of the relationship between insulin resistance and blood pressure remains obscure. Since hypertension does not develop in all insulin resistant subjects and hyperinsulinemia does not always cause a raise in blood pressure, the relationship must be modulated by other genetic or environmental factors.