Work

The vasodilator action of insulin. Implications for the insulin hypothesis of hypertension.

Year: 1993
Type: article
Abstract: The last several years have witnessed tremendousinterest in the hypothesis that insulin resistanceand hyperinsulinemia contribute to the patho-genesis of hypertension. This hypothesis was stimulated by epidemiological studies that demonstrated an asso-ciation between obesity, insulin resistance, and hyper-tension.1-2 Subsequent studies suggested that even lean individuals with essential hypertension have insulin resistance and hyperinsulinemia.3'4 Because hyperinsu-linemia persists during antihypertensive therapy and is not found in secondary renovascular hypertension, the hyperinsulinemia does not appear to be secondary to elevated arterial pressure.5 In addition to effects on glucose metabolism, insulin has sympathetic and renal actions.6-7 In obesity and hypertension, there is resistance to the actions of insulin on glucose uptake but no resistance to the renal and sympathetic actions of insulin. These "secondary " ac-tions of insulin form the basis of the insulin hypothesis of hypertension.8-9 The insulin hypothesis proposes that the compensa-tory hyperinsulinemia that occurs with insulin resis-tance increases sodium reabsorption and sympathetic activity, which combine to cause elevated arterial pres-sure.8-9 An implicit and important assumption of this hypothesis is that, because insulin increases sympathetic noradrenergic activity, it increases vascular resistance and arterial pressure. This editorial will discuss the vasodilator (depressor) action of insulin and the role that this action plays in offsetting the sympathetic and antinatriuretic (pressor) actions of insulin in regulating arterial pressure. The vasodilator actions of insulin have important implica-tions for the insulin hypothesis of hypertension.
Source: Hypertension
Language: English
Field: Medicine
Open Access status: bronze
OpenAlex ID: W1832341580
FWCI: 20.62
Cites: 49
Cited by: 240
Related to: 10