This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ueda, S. Articles by Panza, J. A. Search for Related Content PubMed Articles by Ueda, S. Articles by Panza, J. A.

(Hypertension. 1999;34:e12.)
© 1999 American Heart Association, Inc.

Letters to the Editor

Vasodilator Response to Local Hyperinsulinemia

Shinichiro Ueda

Department of Medicine Yokohama City University School of Medicine, Yokohama, Japan

John R. Petrie; Stephen J. Cleland; Henry L. Elliott; John M.C. Connell

Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland, United Kingdom

	Introduction

 
To the Editor:

Cardillo et al recently reported that systemic but not local hyperinsulinemia causes nitric oxide (NO)-dependent vasodilatation.¹ They suggest that mechanisms stimulated only by systemic but not local hyperinsulinemia contribute to insulin-mediated vasodilatation. We believe that this conclusion is mistaken.

The changes in forearm blood flow during systemic and local hyperinsulinemia in their study were not directly comparable. Thus, although similar concentrations of insulin were achieved in both protocols, there was an artificial dissociation of insulin and glucose levels in the experiment with local hyperinsulinemia: in other words, no glucose supplement was administered in the local experiment, whereas euglycemia was maintained in the systemic study (using the clamp technique). It is likely, therefore, that glucose levels fell in the infused arm in the local experiment and that a discrepancy in forearm glucose uptake between the two conditions may have accounted for the different vasodilator responses to insulin observed.

In support of this alternative explanation, we have consistently shown that intra-arterial infusion of insulin at 5 mU/min (resulting in insulin concentrations of 100 µU/mL in deep venous effluent sampled from the infused forearm), using a strict experimental protocol with a double-blind crossover design and measurement of forearm blood flow ratio (infused: control arm), causes detectable but weak vasodilatation (approximately 20%). In contrast, insulin at the same dose and supplemented by D-glucose at 75 µmol/min (maintaining local venous euglycemia) causes early and significant (50% to 60%) vasodilatation in the human forearm.² This response is not replicated when the stereoisomer L-glucose . . . [Full Text of this Article]

Carmine Cardillo, MD; Julio A. Panza, MD

Cardiology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland