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Institute of Pathophysiology, Semmelweis University of Medicine, Budapest 1445, Hungary; and Department of Physiology, New York Medical College, Valhalla, New York 10595
Skeletal muscle
arterioles dilate in response to increases in flow velocity/wall shear
stress (WSS). The effect of flow/WSS on the diameter of skeletal muscle
venules and the possible endothelial mediation of the response,
however, have not yet been characterized. Thus changes in diameter of
pressurized (10 mmHg) and norepinephrine-preconstricted venules
(179 ± 8 µm in diameter) to increases in perfusate flow before and after endothelium removal or application of inhibitors of NO
and prostaglandin (PG) synthesis,
N
-nitro-L-arginine
(L-NNA,
104 M) and indomethacin (Indo, 2.8 × 105 M), respectively, were
measured. Increases in perfusate flow [elicited by increases in
the pressure difference (Pdiff)
between proximal and distal cannulas] evoked with a delay of 17 ± 2 s dilations, up to 36 ± 9 µm at the highest flow, a
response that was completely eliminated by removal/disruption of the
venular endothelium. Calculation of WSS indicated that in
endothelium-intact venules, the midpoint of the shear stress-diameter
curve was at ~8 dyn/cm2, whereas
in endothelium-denuded vessels, shear stress increased in a linear
fashion with increases in flow, up to 40 dyn/cm2.
L-NNA significantly reduced
flow-induced dilations (from 38 ± 11 to 17 ± 9 µm at 14 mmHg
Pdiff), whereas in the
additional presence of Indo, flow elicited constriction of venules
decreasing basal diameter (by 21 ± 8 µm at
Pdiff 12 mmHg). Thus in skeletal muscle venules an increase in shear stress due to increases in perfusate flow stimulates the release of endothelium-derived NO and PGs
eliciting dilation, which in turn, regulates WSS, albeit at a lower
value than what is observed in arterioles. In the absence of NO and
PGs, flow-induced constriction is revealed, the cause of which remains
obscure. From these data, we propose that shear stress-related
responses of venules are involved in the regulation of venular
resistance, especially during high flow conditions, such as reactive
and exercise hyperemia.
rat gracilis muscle; venular resistance; endothelium-derived constrictor factors; power dissipation
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