{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T08:16:01Z","timestamp":1770884161917,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2013,1,15]]},"abstract":"<jats:p>We examined the hypothesis that \u03b1<jats:sub>1<\/jats:sub>-adrenergic blockade would lead to an inability to correct initial orthostatic hypotension (IOH) and cerebral hypoperfusion, leading to symptoms of presyncope. Twelve normotensive humans (aged 25 \u00b1 1 yr; means \u00b1 SE) attempted to complete a 3-min upright stand, 90 min after the administration of either \u03b1<jats:sub>1<\/jats:sub>-blockade (prazosin, 1 mg\/20 kg body wt) or placebo. Continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv; Doppler), blood pressure (finometer), heart rate, and end-tidal Pco<jats:sub>2<\/jats:sub>were obtained. Compared with placebo, the \u03b1<jats:sub>1<\/jats:sub>-blockade reduced resting mean arterial blood pressure (MAP) (\u221215%; P &lt; 0.01); MCAv remained unaltered ( P \u2265 0.28). Upon standing, although the absolute level of MAP was lower following \u03b1<jats:sub>1<\/jats:sub>-blockade (39 \u00b1 10 mmHg vs. 51 \u00b1 14 mmHg), the relative difference in IOH was negligible in both trials (mean difference in MAP: 2 \u00b1 2 mmHg; P = 0.50). Compared with the placebo trial, the declines in MCAv and Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>during IOH were greater in the \u03b1<jats:sub>1<\/jats:sub>-blockade trial by 12 \u00b1 4 cm\/s and 4.4 \u00b1 1.3 mmHg, respectively ( P \u2264 0.01). Standing tolerance was markedly reduced in the \u03b1<jats:sub>1<\/jats:sub>-blockade trial (75 \u00b1 17 s vs. 180 \u00b1 0 s; P &lt; 0.001). In summary, while IOH was little affected by \u03b1<jats:sub>1<\/jats:sub>-blockade, the associated decline in MCAv was greater in the blockade condition. Unlike in the placebo trial, the extent of IOH and cerebral hypoperfusion failed to recover toward baseline in the \u03b1<jats:sub>1<\/jats:sub>-blockade trial leading to presyncope. Although the development of IOH is not influenced by the \u03b1<jats:sub>1<\/jats:sub>-adrenergic receptor pathway, this pathway is critical in the recovery from IOH to prevent cerebral hypoperfusion and ultimately syncope.<\/jats:p>","DOI":"10.1152\/ajpregu.00427.2012","type":"journal-article","created":{"date-parts":[[2012,11,23]],"date-time":"2012-11-23T01:55:13Z","timestamp":1353635713000},"page":"R147-R154","source":"Crossref","is-referenced-by-count":22,"title":["Initial orthostatic hypotension and cerebral blood flow regulation: effect of \u03b1<sub>1<\/sub>-adrenoreceptor activity"],"prefix":"10.1152","volume":"304","author":[{"given":"Nia C. 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