(Circulation. 2000;101:165.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Cardiology, University of Wales College of Medicine, Cardiff, UK.
Correspondence to Professor M.P. Frenneaux, Department of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK. E-mail daviesja3{at}cardiff.ac.uk
BackgroundAlthough nitric oxide (NO) is known to play an important part in the regulation of arterial tone, little is known about its role in veins. The aim of this study was to investigate the role of basal and stimulated NO activity in the regulation of tone of the human venous capacitance bed.
Methods and ResultsWe measured venous tone using radionuclide forearm venous plethysmography in 24 healthy subjects with no cardiovascular risk factors. In 13 subjects, basal NO activity was assessed by measuring the effects on venous tone of an intra-arterial infusion of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA). In the remaining 11 subjects, stimulated NO activity was evaluated by measuring the effects of an intra-arterial infusion of incremental doses of carbachol, followed in a subgroup by coinfusion with L-NMMA. Infusion of carbachol caused dose-dependent venodilation, with a maximal reduction in forearm venous tone of 40.1±12.5% (P<0.0001). Carbachol-induced venodilation was inhibited by L-NMMA (48.9±6.2% reversal of maximal venodilation, P<0.01). Infusion of L-NMMA alone caused venoconstriction (9.1±6.4% increase in venous tone, P=0.002).
ConclusionsHuman forearm capacitance veins exhibit both stimulated and basal NO activity, which indicates that NO contributes not only to the regulation of venous tone but also to resting venous tone in healthy human subjects.
Key Words: veins endothelium nitric oxide
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