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Diabetes 53:2073-2078, 2004
© 2004 by the American Diabetes Association, Inc.

Vasomotor Responses to Hypoxia in Type 2 Diabetes

Cara J. Weisbrod1, Peter R. Eastwood1,2, Gerard O’Driscoll1,3, Jennifer H. Walsh1, Matthew Best3, John R. Halliwill4, and Daniel J. Green1

1 School of Human Movement and Exercise Science, The University of Western Australia, Crawley, Australia
2 Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Perth, Australia
3 Cardiac Transplant Unit, Department of Cardiology, Royal Perth Hospital, Perth, Australia
4 Department of Exercise and Movement Science, The University of Oregon, Eugene, Oregon

Type 2 diabetes is associated with vascular dysfunction, accelerated atherosclerotic morbidity, and mortality. Abnormal vasomotor responses to chemoreflex activation may contribute to the acceleration of atherosclerotic diabetes complications, but these responses have not previously been investigated. We measured forearm mean blood flow (MBF) and mean vascular conductance (MVC) responses to isocapnic hypoxia in seven healthy and eight type 2 diabetic subjects during local intra-arterial saline infusion and {alpha}-adrenergic blockade (phentolamine). The effects of hypoxia on saline and phentolamine responses significantly differed between groups; relative to normoxia, the %{Delta}MVC with hypoxia during saline was –3.3 ± 11.2% in control and 24.8 ± 13.3% in diabetic subjects, whereas phentolamine increased hypoxic %{Delta}MVC to similar levels (39.4 ± 9.7% in control subjects and 48.0 ± 11.8% in diabetic subjects, P < 0.05, two-way ANOVA). Absolute normoxic MBF responses during saline infusion were 91.9 ± 21.1 and 77.9 ± 15.3 in control and diabetic subjects, respectively, and phentolamine increased normoxic MBF to similar levels (165.2 ± 40.1 ml/min in control subjects and 175.9 ± 32.0 ml/min in diabetic subjects; both P < 0.05). These data indicate that diabetic and control subjects exhibit similar responses to hypoxia in the presence of {alpha}-adrenergic blockade despite evidence of exaggerated {alpha}-mediated vasoconstriction at rest.


Address correspondence and reprint requests to Daniel J. Green, PhD, School of Human Movement and Exercise Science, The University of Western Australia, 35 Stirling Hwy., Crawley, WA 6009, Australia. E-mail: brevis{at}cyllene.uwa.edu.au


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Copyright © 2004 by the American Diabetes Association.