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AJP - Heart and Circulatory Physiology, Vol 258, Issue 6 1918-H1924, Copyright © 1990 by American Physiological Society
ARTICLES |
R. L. Hester
Department of Physiology, University of Mississippi Medical Center, Jackson 39216-4505.
During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.
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