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1 Department of Pharmacology and Physiology, University of Rochester, Rochester, NY, USA
2 Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: ingrid_sarelius{at}urmc.rochester.edu.
The signaling pathways underlying the regulation of vascular resistance by purines in intact microvessels and particularly in communication of remote vasomotor responses are unclear. One process by which remote regions of arterioles communicate is via transmission of signals axially along the vessel wall. In this study we identified a pathway for local and conducted dilations initiated by purines. Adenosine (ADO) or ATP (bind P1 and P2 purinergic receptors respectively) were micropipette applied to arterioles (maximum diameter ~ 40µm) in the cheek pouch of anaesthetized hamsters. Observations were made at the site of stimulation (local) or approx.1200µm upstream along the same vessel. P2 antagonists (PPADS and suramin) inhibited local constriction to ATP while local and upstream dilations were unaffected. In contrast, during inhibition of P1 receptors (with XAC) the local constriction was unchanged while both local and upstream dilations to ATP were inhibited. Hydrolysis of ATP to ADO is implicated in the dilator response as blocking 5' ectonucleotidase (with AOPCP) attenuated ATP induced dilations. Following endothelium denudation, constriction to ATP was unchanged but dilations to both ATP and ADO were inhibited, identifying ECs as the primary target for P1 mediated dilation. Purines increased EC Ca ++ locally and upstream. Chelation of EC Ca++ (with BAPTA) abolished the local and upstream dilations to P1 receptor stimulation. Collectively, these data demonstrate that stimulation of P1 receptors on ECs produces a vasodilation that spreads to remote regions. There is an associated increase in EC Ca ++ , which is a required signaling intermediate in the manifestation of both the local and axially communicated arteriolar dilations.
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