{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T05:40:56Z","timestamp":1788414056965,"version":"build-2803163510"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,9]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Recent studies suggest  that activation of the sympathetic nervous system either directly or  indirectly influences cerebrovascular tone in humans even within the  autoregulatory range. In 6 healthy subjects (aged 29\u00b14 years), we used  transcranial Doppler sonography to determine cerebral  blood flow velocity during sympathetic activation elicited through  head-up tilt (HUT) and sympathetic deactivation through ganglionic  blockade. Pa\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            was manipulated through  hyperventilation and CO\n            <jats:sub>2<\/jats:sub>\n            breathing (5%). With subjects in  the supine position and during HUT, mean arterial pressure  was not influenced by Pa\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            . During ganglionic  blockade, mean arterial pressure decreased markedly with  hyperventilation (\u221213\u00b11.9 mm Hg). Manipulation of sympathetic  tone elicited only mild changes in cerebral blood flow (64\u00b15.8 cm\/s  supine, 58\u00b14.9 cm\/s upright, and 66\u00b16.2 cm\/s during ganglionic  blockade;\n            <jats:italic>P<\/jats:italic>\n            =0.07 by ANOVA). The slope of the regression  between Pa\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            and mean velocity was 1.6\u00b10.18  cm\/(s \u00b7 mm Hg) supine, 1.3\u00b10.14 cm\/(s \u00b7  mm Hg) during HUT, and 2.3\u00b10.36 cm\/(s \u00b7 mm Hg) during  ganglionic blockade (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Spontaneous  Pa\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            and ventilatory response to hypercapnia  were also modulated by the level of sympathetic activity. Changes in  sympathetic tone have a limited effect on cerebral blood flow at normal  Pa\n            <jats:sc>co<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            levels. However, the sympathetic nervous  system seems to attenuate the CO\n            <jats:sub>2<\/jats:sub>\n            -induced increase in  cerebral blood flow. This phenomenon may indicate a moderate direct  effect of the sympathetic nervous system on the cerebral vasculature.  Furthermore, sympathetic activation tends to increase ventilation and  thus can indirectly increase cerebrovascular tone.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.3.383","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"383-388","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":131,"title":["Interaction of Carbon Dioxide and Sympathetic Nervous System Activity in the Regulation of Cerebral Perfusion in Humans"],"prefix":"10.1161","volume":"36","author":[{"given":"Jens","family":"Jordan","sequence":"first","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John R.","family":"Shannon","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andre","family":"Diedrich","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bonnie","family":"Black","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando","family":"Costa","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Robertson","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Italo","family":"Biaggioni","sequence":"additional","affiliation":[{"name":"From the Clinical Research Center, Franz-Volhard Clinic, Humboldt  University, Berlin, Germany (J.J.), and the Autonomic Dysfunction Center,  Vanderbilt University, Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.52.8.962"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.25.12.7974581"},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","unstructured":"Hurn PD Traystman RJ. 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