Endothelium-derived nitric oxide mediates hypoxic vasodilation of
resistance vessels in humans.
Blitzer, Mark L., S. Douglas Lee, Mark A. Creager.
Vascular Medicine and Atherosclerosis Unit, Cardiovascular
Division, Brigham and Women's Hospital, Boston, MA 02115
APStracts 3:0126H, 1996.
Endothelium-derived nitric oxide (EDNO) contributes to basal systemic
vascular resistance under normoxic conditions. The purpose of this
investigation was to determine whether EDNO contributes to the
regulation of limb vascular resistance during hypoxia in healthy
humans. Forearm blood flow was assessed by venous occlusion
plethysmography. Hypoxia was induced by delivering a mixture of N2
and O2 via a gas blender adjusted to reduce the pO2 to 50 mmHg.
During hypoxia, forearm blood flow increased from 2.4 +/- 0.2 to 3.0
+/- 0.3 ml/100 ml/min (p<0.001) and forearm vascular resistance
decreased from 38 +/- 3 to 29 +/- 3 units (p<0.001). The nitric
oxide synthase inhibitor, NG -monomethyl-L-arginine (L-NMMA, 2000
[mu]g/min intra-arterially) was administered to eight subjects. The
percent increase in forearm vascular resistance after L-NMMA was
greater during hypoxia than normoxia (67 +/- 14 versus 39 +/- 15%,
p<0.05). L-NMMA reduced the forearm vasodilator response to
hypoxia from 27 +/- 3 to 11 +/- 5% (p=0.01). To exclude the
possibility that this attenuated response to hypoxia was a
consequence of vasoconstriction and not specific for nitric oxide
synthase inhibition, six subjects received intra-arterial
phenylephrine. Phenylephrine did not affect the vasodilator response
to hypoxia (17 +/- 3 vs. 21 +/-6%, p=NS). It is concluded that EDNO
contributes to hypoxia-induced vasodilation in the forearm resistance
vessels in healthy humans.
Received 1 December 1995; accepted in final form 18 March 1996.
APS Manuscript Number H1123-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96