{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T02:49:15Z","timestamp":1783478955801,"version":"3.55.0"},"reference-count":26,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1999,4]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            \u2014Recent studies have shown that the cerebral arteriolar dilation from hypercapnic acidosis is blocked by agents which inhibit K\n            <jats:sub>ATP<\/jats:sub>\n            channels. These findings suggested that this response is due to opening of K\n            <jats:sub>ATP<\/jats:sub>\n            channels. Because the repose to CO\n            <jats:sub>2<\/jats:sub>\n            is a continuum, with hypercapnic acidosis causing vasodilation and hypocapnic alkalosis causing vasoconstriction, it would be expected that the response to hypocapnic alkalosis would be due to closing of K\n            <jats:sub>ATP<\/jats:sub>\n            channels. There are no studies of the effect of inhibition of K\n            <jats:sub>ATP<\/jats:sub>\n            channels on the response to hypocapnic alkalosis.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            \u2014We investigated the effect of 3 agents that in earlier studies were found to inhibit K\n            <jats:sub>ATP<\/jats:sub>\n            channels\u2014\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>G<\/jats:sup>\n            -nitro-\n            <jats:sc>l<\/jats:sc>\n            -arginine, hydroxylysine, and glyburide\u2014on the cerebral arteriolar constriction caused by graded hypocapnia induced by hyperventilation in anesthetized cats equipped with cranial windows.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            \u2014Hypocapnic alkalosis caused dose-dependent vasoconstriction that was inhibited completely by each of the 3 inhibitors of K\n            <jats:sub>ATP<\/jats:sub>\n            channels. The blockade induced by these agents was eliminated in the presence of topical\n            <jats:sc>l<\/jats:sc>\n            -lysine (5 \u03bcmol\/L).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014The findings show that agents which inhibit ATP-sensitive potassium channels in cerebral arterioles inhibit the vasoconstriction from hypocapnic alkalosis. These and earlier results showing that inhibition of K\n            <jats:sub>ATP<\/jats:sub>\n            channels inhibited dilation from hypercapnic acidosis demonstrate that the response to CO\n            <jats:sub>2<\/jats:sub>\n            in cerebral arterioles is mediated by the opening and closing of K\n            <jats:sub>ATP<\/jats:sub>\n            channels.\n          <\/jats:p>","DOI":"10.1161\/01.str.30.4.851","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:10:52Z","timestamp":1308341452000},"page":"851-854","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Blockade of ATP-Sensitive Potassium Channels in Cerebral Arterioles Inhibits Vasoconstriction From Hypocapnic Alkalosis in Cats"],"prefix":"10.1161","volume":"30","author":[{"given":"Enoch P.","family":"Wei","sequence":"first","affiliation":[{"name":"From the Department of Medicine, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hermes A.","family":"Kontos","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Va."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1994.25"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.271.4.H1498"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.6.3.308"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.4.C974"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.28.2.433"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.78.1.50"},{"key":"e_1_3_2_7_2","first-page":"H1634","volume":"269","year":"1995","unstructured":"Kleppish, T, Nelson, MT. 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