Insulin resistance is a condition which is present in many different diseases all characterized by an increased risk of cardiovascular morbidity and mortality. Generally, the contribution of insulin resistance to the development of cardiovascular pathology is considered to be due to its metabolic consequences. However, recent findings suggest alternative mechanisms by which insulin resistance could exert its role of cardiovascular risk factor. In fact, it has been demonstrated that insulin resistant hypertensive patients have a sympathetic response to euglycemic hyperinsulinemia which is three-fold greater than in normal subjects. This phenomenon could represent an important link between sympathetic nervous system and arterial hypertension. Furthermore, in normal subjects it has been demonstrated that hyperinsulinemia modulates the sympathetic induced vascular response and that this effect is lost in insulin resistant hypertensives. This latter phenomenon could further worsen the consequences of sympathetic overactivity.

[Non-hemodynamic mechanisms of cardiovascular risk in the hypertensive patient: insulin resistance].

IACCARINO, Guido;VECCHIONE, Carmine;
1994-01-01

Abstract

Insulin resistance is a condition which is present in many different diseases all characterized by an increased risk of cardiovascular morbidity and mortality. Generally, the contribution of insulin resistance to the development of cardiovascular pathology is considered to be due to its metabolic consequences. However, recent findings suggest alternative mechanisms by which insulin resistance could exert its role of cardiovascular risk factor. In fact, it has been demonstrated that insulin resistant hypertensive patients have a sympathetic response to euglycemic hyperinsulinemia which is three-fold greater than in normal subjects. This phenomenon could represent an important link between sympathetic nervous system and arterial hypertension. Furthermore, in normal subjects it has been demonstrated that hyperinsulinemia modulates the sympathetic induced vascular response and that this effect is lost in insulin resistant hypertensives. This latter phenomenon could further worsen the consequences of sympathetic overactivity.
1994
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11386/3036093
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