{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T09:28:08Z","timestamp":1774862888542,"version":"3.50.1"},"reference-count":15,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[1991,10,1]],"date-time":"1991-10-01T00:00:00Z","timestamp":686275200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1991,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>To learn more of the role of K+ channel activity in the regulation of pulmonary vascular tone, we compared the pressor effects of the differential blockers of numerous K+ channels, tetraethylammonium chloride and 4-aminopyridine, and the inhibitor of ATP-sensitive K+ channels glibenclamide in meclofenamate-treated salt solution-perfused rat lungs. Tetraethylammonium (1 to 20 mM) and 4-aminopyridine (1 to 10 mM), but not glibenclamide (1 to 20 \u00b5M) caused vasoconstriction in the normoxic lung. The Ca++ channel blocker nifedipine (0.1 \u00b5M) and the alpha adrenoceptor antagonist phentolamine (10 \u00b5M) inhibited the 4-aminopyridine response by about 50% and reduced slightly the smaller tetraethylammonium response. 4-Aminopyridine and, to a lesser extent, tetraethylammonium, but not glibenclamide, also potentiated peak vasoconstriction to angiotensin II and airway hypoxia. Nifedipine, but not phentolamine, inhibited hypoxic vasoconstriction and prevented the potentiation by 4-aminopyridine. These results suggest that Ca++- and\/or voltage-activated (not ATP-sensitive) K++ channels may be important in maintaining low pulmonary vascular tone.<\/jats:p>","DOI":"10.1164\/ajrccm\/144.4.884","type":"journal-article","created":{"date-parts":[[2011,8,3]],"date-time":"2011-08-03T16:19:20Z","timestamp":1312388360000},"page":"884-887","source":"Crossref","is-referenced-by-count":95,"title":["Effects of K+ Channel Blockers on Vascular Tone in the Perfused Rat Lung"],"prefix":"10.1093","volume":"144","author":[{"given":"Kiichi","family":"Hasunuma","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David M.","family":"Rodman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivan F.","family":"Mcmurtry","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1991,10,1]]},"reference":[{"key":"p_8","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1016\/0165-6147(88)90238-6","volume":"9","year":"1988","journal-title":"Pharmacol Sci"},{"key":"p_12","doi-asserted-by":"publisher","DOI":"10.1126\/science.2501869"},{"key":"p_15","first-page":"885","volume":"88","year":"1976","journal-title":"J Lab Clin Invest"},{"key":"p_19","first-page":"184","volume":"5","year":"1983","journal-title":"Pharmacol"},{"key":"p_20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582302"},{"key":"p_28","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(89)90588-8"},{"key":"p_32","doi-asserted-by":"crossref","first-page":"91","DOI":"10.1113\/jphysiol.1989.sp017522","volume":"410","year":"1989","journal-title":"Physiol"},{"key":"p_35","unstructured":"vasodilation in rats. 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