{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T05:03:29Z","timestamp":1787807009764,"version":"build-2784847793"},"reference-count":31,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,6,20]],"date-time":"2014-06-20T00:00:00Z","timestamp":1403222400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>New Findings<\/jats:title><jats:sec><jats:label\/><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p><jats:bold>What is the central question of this study?<\/jats:bold><\/jats:p>\n<jats:p>Muscle sympathetic nerve activity (MSNA) is increased in obstructive sleep apnoea (OSA), leading to hypertension. Is this due to an increase in respiratory\u2013sympathetic coupling, as has been demonstrated in the spontaneously hypertensive rat?<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p><jats:bold>What is the main finding and its importance?<\/jats:bold><\/jats:p>\n<jats:p>Using direct microelectrode recordings of MSNA in hypertensive OSA patients and normotensive control subjects, we show that the magnitude of respiratory modulation is not increased in OSA, arguing against an amplified respiratory\u2013sympathetic coupling as the underlying cause of the neurogenic hypertension, although the temporal coupling of MSNA to respiration was stronger in OSA.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>Obstructive sleep apnoea (OSA) is associated with elevated muscle sympathetic nerve activity (MSNA) during normoxic daytime wakefulness, leading to hypertension. We tested the hypothesis that respiratory\u2013sympathetic coupling, postulated to be the underlying cause of neurogenic hypertension, is increased in OSA. Muscle sympathetic nerve activity, blood pressure, ECG and respiration were recorded in 21 normotensive control subjects and 21 newly diagnosed patients with OSA before and after 6 and 12\u00a0months of treatment with continuous positive airway pressure. Muscle sympathetic nerve activity was recorded via tungsten microelectrodes inserted percutaneously into the peroneal nerve. Cardiac and respiratory modulation of MSNA was quantified from the cross\u2010correlation histograms constructed between the sympathetic spikes and either ECG or respiration. Muscle sympathetic nerve activity was significantly elevated in newly diagnosed OSA patients compared with control subjects (53\u00a0\u00b1\u00a02 <jats:italic>versus<\/jats:italic> 28\u00a0\u00b1\u00a02\u00a0bursts\u00a0min<jats:sup>\u22121<\/jats:sup>). There was a significant fall in MSNA after 6\u00a0months of continuous positive airway pressure (37\u00a0\u00b1\u00a02<jats:bold>\u00a0<\/jats:bold>bursts\u00a0min<jats:sup>\u22121<\/jats:sup>), with no further change after 12\u00a0months (37\u00a0\u00b1\u00a02<jats:bold>\u00a0<\/jats:bold>bursts\u00a0min<jats:sup>\u22121<\/jats:sup>). There were no significant differences in the magnitude of respiratory modulation of MSNA between the OSA patients and control subjects (40\u00a0\u00b1\u00a03.1 <jats:italic>versus<\/jats:italic> 39\u00a0\u00b1\u00a03.4%). However, when considering the normalized temporal profile there were changes in the respiratory patterning of MSNA in OSA, with more activity occurring in postinspiration and less in inspiration and expiration. This was largely reversed following long\u2010term continuous positive airway pressure.<\/jats:p><\/jats:sec>","DOI":"10.1113\/expphysiol.2013.077511","type":"journal-article","created":{"date-parts":[[2014,5,31]],"date-time":"2014-05-31T04:01:44Z","timestamp":1401508904000},"page":"1288-1298","source":"Crossref","is-referenced-by-count":33,"title":["Respiratory modulation of muscle sympathetic nerve activity in obstructive sleep apnoea"],"prefix":"10.1113","volume":"99","author":[{"given":"Rania","family":"Fatouleh","sequence":"first","affiliation":[{"name":"School of Medicine University of Western Sydney  Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David K.","family":"McKenzie","sequence":"additional","affiliation":[{"name":"Department of Respiratory Medicine Prince of Wales Hospital  Sydney NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vaughan G.","family":"Macefield","sequence":"additional","affiliation":[{"name":"School of Medicine University of Western Sydney  Sydney NSW Australia"},{"name":"Neuroscience Research Australia  Sydney NSW 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