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1 Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA
2 Department of Pharmacology and Physiology, University of Rochester, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: ingrid_sarelius{at}urmc.rochester.edu.
Intracellular Ca2+ transients were identified in endothelial cells (ECs) in intact blood perfused arterioles. ECs in cremaster muscle arterioles (diameter ~ 45 µm) in anesthetized mice were loaded with the Ca2+ indicator Fluo-4 (AM) by intraluminal
perfusion, after which blood flow was reestablished. Confocal microscopy was used to visualize Ca2+ as a function of Fluo-4 intensity in real time. Separate sets of experiments were performed under the following conditions: control, ischemia, during inhibition of
P2X or P1 receptors, and with application of exogenous adenosine. In controls, spontaneous EC Ca2+ transients displayed a wide range of activity frequency (1-2 events/minute) and 
one third of these transient events were synchronized between adjacent ECs. The increase in Ca2+ remained localized and did not spread to encompass the entire cell body. Ca2+ transient activity decreased significantly with ischemia (from
9.9±0.6 to 3.1±0.3 events/min, n=135), but was unaffected by P2X or P1 receptor inhibition. Exogenous adenosine significantly increased the frequency of Ca2+ transients
(to 12.8±0.9 events/min) and increased synchronization so that 50% of all Ca2+ events
were synchronized between ECs. This response to adenosine was not due to an increase in shear stress. These data indicate that localized Ca2+ transients are sensitive to flow conditions and, separately, to metabolically active pathways (exogenous adenosine),
although the basal activity occurs independently of P2X or P1 receptors. These transients
may represent a mechanism by which individual EC responses are integrated to result in coordinated arteriolar responses in situ.
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