{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T18:48:57Z","timestamp":1793040537061,"version":"4.5.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p> 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 P<jats:sub>1<\/jats:sub> and P<jats:sub>2<\/jats:sub> purinergic receptors, respectively) was micropipette applied to arterioles (maximum diameter \u223c40 \u03bcm) in the cheek pouch of anesthetized hamsters. Observations were made at the site of stimulation (local) or \u223c1,200 \u03bcm upstream along the same vessel. P<jats:sub>2<\/jats:sub> antagonists (pyridoxalphosphate-6-azophenyl-2\u2032,4\u2032-disulfonic acid tetrasodium and suramin) inhibited local constriction to ATP, whereas local and upstream dilations were unaffected. In contrast, during inhibition of P<jats:sub>1<\/jats:sub> 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\u2032-ectonucleotidase (with \u03b1,\u03b2-methyleneadenosine 5\u2032-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 P<jats:sub>1<\/jats:sub>-mediated dilation. Purines increased EC Ca<jats:sup>2+<\/jats:sup> locally and upstream. Chelation of EC Ca<jats:sup>2+<\/jats:sup> (with BAPTA) abolished the local and upstream dilations to P<jats:sub>1<\/jats:sub> receptor stimulation. Collectively, these data demonstrate that stimulation of P<jats:sub>1<\/jats:sub> receptors on ECs produces a vasodilation that spreads to remote regions. There is an associated increase in EC Ca<jats:sup>2+<\/jats:sup>, which is a required signaling intermediate in the manifestation of both the local and axially communicated arteriolar dilations. <\/jats:p>","DOI":"10.1152\/ajpheart.00788.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:10:42Z","timestamp":1425395442000},"page":"H26-H37","source":"Crossref","is-referenced-by-count":68,"title":["Conducted dilations initiated by purines in arterioles are endothelium  dependent and require endothelial Ca<sup>2+<\/sup>"],"prefix":"10.1152","volume":"285","author":[{"given":"Tasmia","family":"Duza","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingrid H.","family":"Sarelius","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1016\/0163-7258(94)00048-4"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1997.272.6.H2693"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/26.1.40"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702775"},{"key":"REF5","unstructured":"Burnstock G. 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