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This Article Full Text Full Text (PDF) All Versions of this Article: 573/1/133    most recent jphysiol.2006.106500v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kelly, R. Articles by Snow, H. M. Search for Related Content PubMed PubMed Citation Articles by Kelly, R. Articles by Snow, H. M. Related Collections Cardiovascular

¹ Biological Services Unit and Department of Physiology, University College Cork, Ireland
² Cardiovascular Medicine, Department of Medicine and Therapeutics, University of Aberdeen, UK
³ School of Pharmacy, Robert Gordon University, Aberdeen, UK

Clinical hyperglycaemia affects vascular endothelial function, but the effect on shear stress-induced arterial dilatation has not yet been established. We hypothesized that hyperglycaemia would inhibit this response via impaired glycocalyx mechanotransduction. Experiments were carried out in the anaesthetized pig in which pressure, blood flow and diameter of the left iliac artery were measured at two sites: proximal (d1) and distal (d2). Infusion of glucose, sufficient to raise blood glucose to 16–30 mM along the whole length of the artery, attenuated the shear stress-dependent dilatation in both sections of the artery with preservation of the responses to acetylcholine. The distal site was then isolated using snares and the lumen exposed to blood containing 25–35 mM glucose for 20 min. In the control situation, after exposure of both sections to normoglycaemia (5.7 mM glucose), both sections of artery showed increases in diameter in response to shear stress and acetylcholine. Hyperglycaemia attenuated the shear stress-dependent dilatation in the distal section only (P < 0.25), but not the response to acetylcholine. It is concluded from these results that the hyperglycaemia-impaired dilatation is consistent with loss of mechanotransducing properties of the endothelial glycocalyx by hyperglycaemia. These findings offer a possible explanation for the increased incidence of vascular disease in diabetic patients.

(Received 31 January 2006; accepted after revision 9 March 2006; first published online 16 March 2006)
Corresponding author R. Kelly: Biological Services Unit, University College Cork, Cork, Ireland. Email: rokelly81{at}gmail.com

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