APStracts 2:0500H, 1995.

Nitric oxide release in rat skeletal muscle capillary. Mitchell, Debra, and Karel Tyml. John P. Robarts Research Institute and Departments of Medical Biophysics and Pharmacology and Toxicology, The University of Western Ontario, London, Canada

APStracts 2:0500H, 1995.

Nitric oxide (NO) has been shown to be a potent vasodilator released from endothelial cells (EC) in large blood vessels, but NO release has not been examined in the capillary bed. Since the capillary bed represents the largest source of EC, it may be the largest source of vascular NO. In the present study, we used intravital microscopy to examine the effect of the nitric oxide synthase inhibitor, NG-nitro -L-arginine methyl ester (L-NAME) on the microvasculature of the rat extensor digitorum longus muscle. L-NAME (30 mM) locally applied to a capillary (300 [mu]m from the feeding arteriole) significantly reduced red blood cell velocity (VRBC; control VRBC=238+/-58 SE [mu]m/s; DVRBC=-76+/-8%) and red cell flux (4.4 +/- 0.7 to 2.8 +/- 0.7 RBC/s) in the capillary, but did not change feeding arteriole diameter (Dcon=6.3+/-0.7 [mu]m, DD=5+/-7%) or draining venule diameter (Dcon=10.1+/-0.6 [mu]m, DD=4+/-2%). In view of the VRBC change, the flux reduction was equivalent to an increased local hemoconcentration from 1.8 to 5 RBC's per 100 [mu]m capillary length. L-NAME also caused an increase in the number of adhering leukocytes in the venule from 0.29 to 1.43/100 [mu]m. L-NAME (30 mM) applied either to arterioles or to venules did not change capillary VRBC. Bradykinin (BK) locally applied to the capillary caused significant increases in VRBC (DVRBC=111+/-23%) and in arteriolar diameter (DD=40+/-5%). This BK response was blocked by capillary pre-treatment with 30 mM L-NAME (DVRBC=-4+/-27%; DD=5+/-9% after BK). We concluded that NO may be released from capillary EC both basally and in response to the vasodilator BK. We hypothesise that (i) low basal levels of NO affect capillary blood flow by modulating local hemoconcentration and leukocyte adhesion, and (ii) higher levels of NO (stimulated by BK) may cause a remote vasodilation to increase microvascular blood flow.

Received 20 March 1995; accepted in final form 6 October 1995.
APS Manuscript Number H268-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95