This Article Full Text Full Text (PDF) All Versions of this Article: 44/5/618    most recent 01.HYP.0000144802.18301.2fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Adair, T. H. Search for Related Content PubMed PubMed Citation Articles by Adair, T. H. Related Collections Angiogenesis

(Hypertension. 2004;44:618.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

An Emerging Role for Adenosine in Angiogenesis

From the Angiogenesis Research Laboratories, Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson.

Correspondence to Thomas H. Adair, Angiogenesis Research Laboratories, Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 33216-4505. E-mail Tadair@physiology.umsmed.edu

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

The possibility that adenosine has an important role in cardiovascular function was introduced 75 years ago when Drury and Szent-Gyorgyi¹ found that extracts from heart and other tissues produced vasodilation, hypotension, bradycardia, and a decrease in atrioventricular conduction velocity. In the early 1960s, Berne et al² proposed the so-called retaliatory metabolite concept in which hypoxic tissues produce adenosine from ATP, and the adenosine in turn functions to restore a balance between oxygen demand and oxygen supply by causing vasodilation and increased blood flow. This has been shown to be true for heart, brain, and skeletal muscle in several different species.² Adenosine thus serves as a negative feedback signal to maintain tissue oxygenation within a normal range.

Mounting evidence suggests that adenosine may also have a long-term role to increase tissue oxygenation by stimulating the growth of blood vessels. Physiological concentrations of adenosine or adenosine agonists cause a dose-related increase in the proliferation of endothelial cells obtained from bovine aorta,³ bovine coronary venules,³ and human umbilical veins,^4,5 but they have no effect on the proliferation of human fibroblasts⁴ and rat myocardial myoblasts.⁵ Also, raising endogenous levels of adenosine by inhibition of adenosine kinase can stimulate the proliferation of human endothelial cells obtained from umbilical veins.⁵ Adenosine stimulates angiogenesis in the body and chorioallantoic membrane of the chick embryo and could mediate a portion of the hypoxia-induced angiogenesis in the same tissues.⁶ Early work has also shown that prolonged infusion of adenosine induces angiogenesis in rabbit heart and skeletal muscle.⁷ That adenosine . . . [Full Text of this Article]

This article has been cited by other articles:

				Y. Hellsten, N. Rufener, J. J. Nielsen, B. Hoier, P. Krustrup, and J. Bangsbo Passive leg movement enhances interstitial VEGF protein, endothelial cell proliferation, and eNOS mRNA content in human skeletal muscle Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2008; 294(3): R975 - R982. [Abstract] [Full Text] [PDF]

				L. Macedo, G. Pinhal-Enfield, V. Alshits, G. Elson, B. N. Cronstein, and S. J. Leibovich Wound Healing Is Impaired in MyD88-Deficient Mice: A Role for MyD88 in the Regulation of Wound Healing by Adenosine A2A Receptors Am. J. Pathol., December 1, 2007; 171(6): 1774 - 1788. [Abstract] [Full Text] [PDF]