{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T04:26:51Z","timestamp":1769747211371,"version":"3.49.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2002,3]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Background and Purpose<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Potassium channels or nitric oxide or both are major mediators of acidosis-induced dilation in the cerebral circulation. However, these contributions depend on a variety of factors such as species and vessel location. The present study was designed to clarify whether potassium channels and endothelial nitric oxide are involved in acidosis-induced dilation of isolated rat cerebral arterioles.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Methods<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Cerebral arterioles were cannulated and monitored with an inverted microscope. Acidosis (pH 6.8 to 7.4) produced by adding hydrogen ions mediated dilation of the cerebral arterioles in a concentration-dependent manner. The role of nitric oxide and potassium channels in response to acidosis was examined with several specific inhibitors and endothelial damage.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Results<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            The dilation was significantly inhibited by potassium chloride (30 mmol\/L) and glibenclamide (3 \u03bcmol\/L; ATP-sensitive potassium channel inhibitor). We found that 30 \u03bcmol\/L BaCl\n            <jats:sub>2<\/jats:sub>\n            (concentration-dependent potassium channel inhibitor) also affected the dilation; however, an additional treatment of 3 \u03bcmol\/L glibenclamide did not produce further inhibition. Tetraethylammonium ion (1 mmol\/L; calcium-activated potassium channel inhibitor) and 4-aminopyridine (100 \u03bcmol\/L; voltage-dependent potassium channel inhibitor) as well as ouabain (10 \u03bcmol\/L; Na-K ATPase inhibitor) and\n            <jats:italic>N<\/jats:italic>\n            -methylsulphonyl-6-(2-proparglyloxyphenyl) hexanamide (1 \u03bcmol\/L; cytochrome P450 epoxygenase inhibitor) did not alter acidotic dilation.\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>\u03c9<\/jats:sup>\n            -Monomethyl-\n            <jats:sc>l<\/jats:sc>\n            -arginine (10 \u03bcmol\/L) and\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>\u03c9<\/jats:sup>\n            -nitro-\n            <jats:sc>l<\/jats:sc>\n            -arginine (10 \u03bcmol\/L) as nitric oxide synthase inhibitor blunted the dilation. Furthermore, the dilation was significantly attenuated after the endothelial impairment. Additional treatment with glibenclamide (3 \u03bcmol\/L) further reduced the dilation in response to acidosis.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Conclusions<\/jats:italic>\n                <\/jats:bold>\n                \u2014\n              <\/jats:italic>\n            <\/jats:bold>\n            Endothelial nitric oxide and smooth muscle ATP-sensitive potassium channels contribute to acidosis-induced dilation of rat cerebral arterioles. Endothelial damage caused by pathological conditions such as subarachnoid hemorrhage or traumatic brain injury may contribute to reduced blood flow despite injury-induced cerebral acidosis.\n          <\/jats:p>","DOI":"10.1161\/hs0302.104112","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"844-849","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":36,"title":["Role of Endothelial Nitric Oxide and Smooth Muscle Potassium Channels in Cerebral Arteriolar Dilation in Response to Acidosis"],"prefix":"10.1161","volume":"33","author":[{"given":"Tetsuyoshi","family":"Horiuchi","sequence":"first","affiliation":[{"name":"From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo (T.H., H.H.D., R.G.D.), and Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan (K.H., T.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans H.","family":"Dietrich","sequence":"additional","affiliation":[{"name":"From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo (T.H., H.H.D., R.G.D.), and Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan (K.H., T.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuhiro","family":"Hongo","sequence":"additional","affiliation":[{"name":"From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo (T.H., H.H.D., R.G.D.), and Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan (K.H., T.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuya","family":"Goto","sequence":"additional","affiliation":[{"name":"From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo (T.H., H.H.D., R.G.D.), and Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan (K.H., T.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"Jr","given":"Ralph G.","family":"Dacey","sequence":"additional","affiliation":[{"name":"From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo (T.H., H.H.D., R.G.D.), and Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan (K.H., T.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1997.00263.x"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1159\/000159163"},{"key":"e_1_3_2_3_2","first-page":"H598","volume":"243","year":"1982","unstructured":"Dacey RG Jr, Duling BR. 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