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Department of Physiology, New York Medical College, Valhalla, New York 10595
The
purpose of this study was to investigate the mechanism underlying
arteriolar responses to hyperosmolality and to determine the effects of
daily exercise on this response. Dilator responses were measured in
isolated, cannulated, and pressurized skeletal muscle arterioles.
Osmolality was increased from ~290 to 330 mosmol/kgH2O by
adding glucose, sucrose, or mannitol to the superfusion solution. All
three compounds elicited similar changes in vessel diameter, suggesting
that this response was due to changes in osmolality. Responses to
glucose were abolished by endothelium removal but were not altered in
endothelium-intact vessels by superfusion with the nitric oxide
synthase inhibitor
N
-nitro-L-arginine or the
cyclooxygenase inhibitor indomethacin. In endothelium-intact
arterioles, responses to glucose superfusion with the ATP-sensitive
potassium (KATP) channel inhibitor glibenclamide; however,
intraluminal perfusion with glibenclamide nearly abolished the
responses to glucose and mannitol. Intraluminal administration of
glucose elicited a significantly greater dilation than extraluminal glucose. The response to intraluminal glucose was also inhibited by
intraluminal glibenclamide. Four weeks of daily exercise did not
significantly alter the responses to hyperosmolality in gracilis or
soleus muscle arterioles. These data demonstrate that physiological increases in intraluminal osmolality dilate rat skeletal muscle arterioles via activation of endothelial KATP channels;
however, this endothelium-dependent response is not augmented by daily exercise.
skeletal muscle arterioles; glibenclamide; glucose; microcirculation; potassium channels
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