{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T00:12:56Z","timestamp":1782778376950,"version":"3.54.5"},"reference-count":41,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL127071"],"award-info":[{"award-number":["HL127071"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p> The role of the sympathetic nervous system in cerebral blood flow (CBF) regulation remains unclear. Previous studies have primarily measured middle cerebral artery blood velocity to assess CBF. Recently, there has been a transition toward measuring internal carotid artery (ICA) and vertebral artery (VA) blood flow using duplex Doppler ultrasound. Given that the VA supplies autonomic control centers in the brainstem, we hypothesized that graded sympathetic activation via lower body negative pressure (LBNP) would reduce ICA but not VA blood flow. ICA and VA blood flow were measured during two protocols: protocol 1, low-to-moderate LBNP (\u221210, \u221220, \u221230, and \u221240 Torr) and protocol 2, moderate-to-high LBNP (\u221230, \u221250, and \u221270 Torr). ICA and VA blood flow, diameter, and blood velocity were unaffected up to \u221240 LBNP. However, \u221250 and \u221270 LBNP evoked reductions in ICA and VA blood flow [e.g., \u221270 LBNP: percent change (%\u2206)VA-baseline = \u221227.6 \u00b1 3.0] that were mediated by decreases in both diameter and velocity (e.g., \u221270 LBNP: %\u2206VA-baseline diameter = \u22127.5 \u00b1 1.9 and %\u2206VA-baseline velocity = \u221213.6 \u00b1 1.7), which were comparable between vessels. Since hyperventilation during \u221270 LBNP reduced end-tidal pressure of carbon dioxide ([Formula: see text]), this decrease in [Formula: see text] was matched via voluntary hyperventilation. Reductions in ICA and VA blood flow during hyperventilation alone were significantly smaller than during \u221270 LBNP and were primarily mediated by decreases in velocity (%\u2206VA-baseline velocity = \u22128.6\u2009\u00b1\u20092.4 and %\u2206VA-baseline diameter = \u22120.05\u2009\u00b1\u20090.56). These data demonstrate that both ICA and VA were unaffected by low-to-moderate sympathetic activation, whereas robust reflex-mediated sympathoexcitation caused similar magnitudes of vasoconstriction in both arteries. Thus, contrary to our hypothesis, the ICA was not preferentially vasoconstricted by sympathetic activation. <\/jats:p><jats:p> NEW &amp; NOTEWORTHY Our study demonstrates that moderate-to-high reflex-mediated sympathetic activation with lower body negative pressure (LBNP) decreases internal carotid artery and vertebral artery blood flow via reductions in both vessel diameter and blood velocity. This vasoconstriction was primarily sympathetically mediated as voluntary hyperventilation alone, to isolate the effect of decreases in end-tidal pressure of carbon dioxide that occurred during LBNP, resulted in a significantly smaller vasoconstriction. In contrast to our hypothesis, these data indicate a lack of heterogeneity between the anterior and posterior cerebral circulations in response to sympathoexcitation. <\/jats:p>","DOI":"10.1152\/japplphysiol.00623.2018","type":"journal-article","created":{"date-parts":[[2018,9,6]],"date-time":"2018-09-06T15:43:49Z","timestamp":1536248629000},"page":"1779-1786","source":"Crossref","is-referenced-by-count":19,"title":["Regulation of regional cerebral blood flow during graded reflex-mediated sympathetic activation via lower body negative pressure"],"prefix":"10.1152","volume":"125","author":[{"given":"Jasdeep","family":"Kaur","sequence":"first","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer R.","family":"Vranish","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5776-3824","authenticated-orcid":false,"given":"Thales C.","family":"Barbosa","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takuro","family":"Washio","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Toyo University, Kawagoe-shi, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin E.","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandi Y.","family":"Stephens","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, University of Texas at Arlington, Arlington, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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