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Conducted dilations initiated by purines in arterioles are endothelium dependent and require endothelial Ca²⁺

¹Department of Biomedical Engineering and ²Department of Pharmacology and Physiology, University of Rochester, Rochester, New York 14642

Submitted 6 September 2002 ; accepted in final form 11 March 2003

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) was micropipette applied to arterioles (maximum diameter 40 µm) in the cheek pouch of anesthetized hamsters. Observations were made at the site of stimulation (local) or 1,200 µm upstream along the same vessel. P₂ antagonists (pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid tetrasodium and suramin) inhibited local constriction to ATP, whereas local and upstream dilations were unaffected. In contrast, during inhibition of P₁ receptors (with xanthine amine congener) the local constriction was unchanged, whereas 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 ,-methyleneadenosine 5'-diphosphate) attenuated ATP-induced dilations. After endothelium denudation, constriction to ATP was unchanged, but dilations to both ATP and Ado were inhibited, identifying endothelial cells (ECs) as the primary target for P₁-mediated dilation. Purines increased EC Ca²⁺ locally and upstream. Chelation of EC Ca²⁺ (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 Ca²⁺, which is a required signaling intermediate in the manifestation of both the local and axially communicated arteriolar dilations.

conducted response; endothelium-dependent dilation; microvascular communication

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