Published online before print September 28, 2009, doi: 10.1161/HYPERTENSIONAHA.109.141176
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(Hypertension. 2009;54:960.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
Exogenous Ghrelin on Nitric Oxide-Endothelin 1 Imbalance in Metabolic Syndrome
Can We Kill 2 Birds With 1 Stone?
From the Department of Internal Medicine, University of Pisa, Pisa, Italy.
Correspondence to Stefano Taddei, Department of Internal Medicine, University of Pisa, via Roma 67, 56100 Pisa, Italy. E-mail s.taddei@int.med.unipi.it
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Ghrelin is a recently identified growth hormone-releasing peptide, isolated from the stomach, initially described as an endogenous ligand for growth hormone secretagogue receptors. Although essentially a gastric hormone, which is involved in regulating energy balance and exerts influence on the pituitary-gonadal axis, additional growth hormone-independent cardiovascular actions have been attributed recently to this peptide. Among others, a significant impact on endothelial function has been identified, because ghrelin receptor expression has been documented in human endothelial cells.1 Experimental reports indicated that exogenous ghrelin administration ameliorates endothelial dysfunction and reduces the vasoconstrictor effect of endothelin 1 (ET-1) and, at higher doses, also decreases arterial pressure.
Obese patients with metabolic syndrome are characterized by reduced circulating ghrelin levels.2 These findings, together with evidence of compromised NO availability and enhanced ET-1-mediated vasoconstriction,3 make obesity a useful experimental model for investigating the impact of ghrelin on NO and ET-1.
In this issue of Hypertension, Tesauro et al4 investigated whether exogenous ghrelin may exert a beneficial effect on NO and ET-1 imbalance in the forearm microcirculation of patients with obesity-related metabolic syndrome. NO availability was assessed by intra-arterial infusion of the NO synthase inhibitor NG-monomethyl-L-arginine, whereas ET-1-mediated vasoconstriction was investigated by using the ETA receptor antagonist BQ-123. In basal conditions, patients showed a higher vasodilating response to BQ-123 and a reduced contracting effect of NG-monomethyl-L-arginine as compared with controls, suggesting predominantly ET-1-mediated vasoconstriction and a reduced NO vasodilator effect in this clinical condition. The novel aspect of the study
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