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(Hypertension. 2005;45:347.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Insulin and Blood Pressure

Connected on a Circumference?

From the Department of Internal Medicine and C.N.R. Institute of Clinical Physiology, University of Pisa School of Medicine, Pisa, Italy.

Correspondence to Ele Ferrannini, University of Pisa, Department of Internal Medicine, Via Savi, 8, Pisa 56100 Italy. E-mail ferranni@ifc.cnr.it

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Hypertension has long been known to be more prevalent among obese subjects or in patients with diabetes, ie, in states of insulin resistance.¹ After the demonstration that essential hypertension is an insulin-resistant state in its own right,² it was logical to include hypertension in the insulin resistance syndrome,³ later transmuted into the metabolic syndrome.⁴ A large number of studies, both epidemiological and physiological, have explored this association and, more in general, the interrelationships between blood pressure and insulin action. Summarizing the available evidence—and critically analyzing its merits and pitfalls—is beyond the scope of this brief commentary. It may be nevertheless useful to recall a few general points. First, the association between insulin resistance and hypertension extends into the normal state as an association between insulin action on glucose metabolism and blood pressure levels⁵; this clearly speaks for the existence of multiple cross-talk between the 2 homeostatic systems. Second, longitudinal studies have confirmed that insulin resistance (as measured by its surrogate, fasting hyperinsulinemia) may precede the development of frank hypertension.⁶ The reverse temporal sequence, ie, hypertension antedating insulin resistance, has not been documented. Third, associations, even if fairly consistent, do not mean necessarily one-on-one relationships (such that every insulin-resistant individual is, or will become, hypertensive); most commonly, they stand for overlapping clinical phenotypes. Fourth, contrary to habitual disclaimers, consistent associations do imply mechanisms; however, mechanisms need not be unique and direct: they may be multiple and/or indirect, and they must be identified experimentally. For example, hyperinsulinemia activates the adrenergic nervous . . . [Full Text of this Article]

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