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J Appl Physiol 81: 2105-2114, 1996;
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Journal of Applied Physiology
Vol. 81, No. 5, pp. 2105-2114, November 1996
EXERCISE AND MUSCLE

Endothelial cell dilatory pathways link flow and wall shear stress in an intact arteriolar network

Mary D. S. Frame and Ingrid H. Sarelius

Department of Biophysics, University of Rochester, Rochester, New York 14642

Received 19 June 1996; accepted in final form 20 June 1996.

Frame, Mary D. S., and Ingrid H. Sarelius. Endothelial cell dilatory pathways link flow and wall shear stress in an intact arteriolar network. J. Appl. Physiol. 81(5): 2105-2114, 1996.---Our purpose was to determine whether the endothelial cell-dependent dilatory pathways contribute to the regulation of flow distribution in an intact arteriolar network. Cell flow, wall shear stress (Tomega ), diameter, and bifurcation angle were determined for four sequential branches of a transverse arteriole in the superfused cremaster muscle of pentobaribtal sodium (Nembutal, 70 mg/kg)-anesthetized hamsters (n = 51). Control cell flow was significantly greater into upstream than into downstream branches [1,561 ± 315 vs. 971 ± 200 (SE) cells/s, n = 12]. Tissue exposure to 50 µM Nomega -nitro-L-arginine + 50 µM indomethacin (L-NNA + Indo) produced arteriolar constriction of 14 ± 4% and decreased flow into the transverse arteriole. More of the available cell flow was diverted to downstream branches, yet flow distribution remained unequal. Control Tomega was higher upstream than downstream (31.3 ± 6.8 vs. 9.8 ± 1.5 dyn/cm2). L-NNA + Indo decreased Tomega upstream and increased Tomega downstream to become equal in all branches, in contrast to flow. To determine whether constriction in general induced the same changes, 5% O2 (8 ± 4% constriction) or 10-9 M norepinephrine (NE; 4 ± 3% constriction) was added to the tissue (n = 7). With O2, flow was redistributed to become equal into each branch. With NE, flow decreased progressively more into the first three branches. The changes in flow distribution were thus predictable and dependent on the agonist. With O2 or NE, the spatial changes in flow were mirrored by spatial changes in Tomega . Changes in diameter and in cell flux were not related for L-NNA + Indo (r = 0.45), O2 (r = 0.07), or NE (r = 0.36). For all agonists, when the bifurcation angle increased, cell flow to the branch decreased significantly, whereas if the angle decreased, flow was relatively preserved; thus active changes in bifurcation angle may influence red cell distribution at arteriolar bifurcations. Thus, when the endothelial cell dilatory pathways were blocked, the changes in flow and in Tomega were uncoupled; yet when they were intact, flow and Tomega changed together.

flow-dependent responses; capillary recruitment; bifurcation angle; nitric oxide


0161-7567/96 $5.00 Copyright © 1996 the American Physiological Society




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