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Articles in PresS, published online ahead of print August 20, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00333.2002
Submitted on July 23, 2002
Accepted on August 18, 2002
1 Department of Kinesiology and Applied Physiology, University of Colorado, Boulder, CO, USA
2 Division of Cardiology, University of Colorado Health Sciences Center, Denver, CO, USA
3 Department of Kinesiology and Applied Physiology, University of Colorado, Boulder, CO, USA; Department of Medicine, Division of Geriatrics, University of Colorado, Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: desouzac{at}colorado.edu.
We determined the influence of oral contraceptives (OC) on the capacity of the endothelium to release tissue-type plasminogen activator (t-PA). Twenty-three healthy premenopausal women were studied: 12 non-users and 11 users of OC. Net endothelial release rates of t-PA were calculated as the product of the arteriovenous concentration gradient and forearm plasma flow in response to intra-arterial bradykinin (BK: 12.5-50 ng/100 mL tissue/min) and sodium nitroprusside (NTP: 1.0-4.0 µg/100 mL tissue/min). Net release of t-PA antigen and increment in t-PA activity across the forearm to BK increased (P<0.01) in a dose-dependent fashion and to similar extents in the non-users and users of OC. At the highest BK dose net release of t-PA antigen was 64.5±8.2 and 66.2±15.4 ng/100 mL tissue/min in the non-users and users of OC; whereas the net increment in t-PA activity was 18.6±3.0 and 16.0±2.0 IU/100 mL tissue/min, respectively. There was no effect of NTP on t-PA release in either group. These results indicate that endothelial t-PA release is not altered in premenopausal women who use oral contraception.
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