{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T07:56:21Z","timestamp":1793692581433,"version":"4.5.1"},"reference-count":59,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,10,24]],"date-time":"2005-10-24T00:00:00Z","timestamp":1130112000000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:p>\n                    Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor\u2013vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied 11 healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of \u221240 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus\u2013response curves were defined during (i) air breathing, (ii) hypoxia (12% O\n                    <jats:sub>2<\/jats:sub>\n                    in N\n                    <jats:sub>2<\/jats:sub>\n                    ), and (iii) hypercapnia (5% CO\n                    <jats:sub>2<\/jats:sub>\n                    in 95% O\n                    <jats:sub>2<\/jats:sub>\n                    ). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to \u2018set point\u2019). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post\u2010stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or \u2018set point\u2019 for the control of RR interval, heart rate or mean arterial pressure. Peak sensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from \u22122.5 \u00b1 0.4 units to \u22121.4 \u00b1 0.1 units (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05) and this was restored in the post\u2010stimulus period to \u22122.6 \u00b1 0.5 units. There was no effect on \u2018set point\u2019. Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post\u2010stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post\u2010control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, \u2018set point\u2019 was significantly increased from 74.7 \u00b1 4 to 87.0 \u00b1 2 mmHg (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.02). This was not completely restored to pre\u2010stimulus control levels in the post\u2010stimulus control period (82.2 \u00b1 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor\u2013vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex \u2018set point\u2019. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemoreceptors on baroreflex function may contribute to promoting hypertension in patients with obstructive sleep apnoea.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2005.094151","type":"journal-article","created":{"date-parts":[[2005,8,18]],"date-time":"2005-08-18T20:13:22Z","timestamp":1124396002000},"page":"677-687","source":"Crossref","is-referenced-by-count":121,"title":["Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia \u2013 a mechanism for promoting hypertension in obstructive sleep apnoea"],"prefix":"10.1113","volume":"568","author":[{"given":"V. L.","family":"Cooper","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. B.","family":"Pearson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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