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Pulmonary venous rings (500-\u03bcm external diameter) were isolated from 1-wk-old piglets and precontracted with the thromboxane mimetic U-46619. Responses to hypocapnic alkalosis were then measured under control conditions after inhibition of endothelium-derived modulator activity or K<jats:sup>+<\/jats:sup>channels. In control rings, alkalosis caused a 34.4 \u00b1 4.8% decrease in the U-46619-induced contraction. This relaxation was significantly blunted in rings without functional endothelium and in rings treated with nitric oxide synthase or guanylate cyclase inhibitors. However, neither cyclooxygenase inhibition nor voltage-dependent, calcium-dependent, or ATP-dependent K<jats:sup>+<\/jats:sup>-channel inhibitors altered alkalosis-induced relaxation. These data suggest that alkalosis caused significant dilation of piglet pulmonary veins that was mediated by the nitric oxide-cGMP pathway.<\/jats:p>","DOI":"10.1152\/ajplung.2000.278.5.l968","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T00:34:27Z","timestamp":1514075667000},"page":"L968-L973","source":"Crossref","is-referenced-by-count":8,"title":["Mediators of alkalosis-induced relaxation of piglet pulmonary veins"],"prefix":"10.1152","volume":"278","author":[{"given":"Ted R.","family":"Halla","sequence":"first","affiliation":[{"name":"Departments of Pediatrics and Neurology, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane A.","family":"Madden","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Neurology, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, Milwaukee, 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