Copyright © 2003 by the European Society of Cardiology.
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Visceral obesity is characterized by impaired nitric oxide-independent vasodilation
Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy
* Correspondence to: Angelo Avogaro, MD, Cattedra di Malattie del Metabolismo, Via Giustiniani 2, 35128 Padova, Italy. Tel: 39-049-8212178; Fax: 39-049-8754179
E-mail address: angelo.avogaro{at}unipd.it
Received 29 November 2002; revised 31 March 2003; accepted 3 April 2003
Background Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm.
Methods and results In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na+/K+ATPase inhibitor) alone or (5) in combination with BaCl2(KIRinhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P<0.01). Irrespective of prostaglandins and nitric oxide inhibition, bradykinin response was lower in the viscerally obese. Intrabrachial potassium determined a significantly blunted response (P<0.05). Ouabain caused a similar, moderate decrease in basal FBF in the two groups; the coinfusion of BaCl2caused a more intense decline in FBF which was significantly relevant in obese (–24±5%, P<0.01).
Conclusions In obese patients there is a blunted nitric oxide-independent relaxation determined by a decreased response of inwardly rectifying potassium channels.
Key Words: Endothelium • Endothelium-derived hyperpolarizing factor • Obesity • Insulin resistance • Potassium channels
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