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This Article Full Text Full Text (PDF) All Versions of this Article: 91/5/907    most recent expphysiol.2005.033084v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moore, J. P. Articles by Hainsworth, R. Search for Related Content PubMed PubMed Citation Articles by Moore, J. P. Articles by Hainsworth, R. Related Collections Cardiovascular control

¹ Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK ² Department of Physiological Sciences, Universidad Peruana Cayetano Heredia, Lima 100, Peru ³ New Mexico Health Enhancement and Marathon Clinics Research Foundation, Alburquerque, NM87122, USA

We investigated carotid baroreflex control of vascular resistance in two groups of high-altitude natives: healthy subjects (HA) and a group with chronic mountain sickness (CMS), a maladaptation condition characterized by high haematocrit values and symptoms attributable to chronic hypoxia. Eleven HA controls and 11 CMS patients underwent baroreflex testing, using the neck collar method in which the pressure distending the carotid baroreceptors was changed by applying pressures of –40 to +60 mmHg to the chamber. Responses of forearm vascular resistance were assessed from changes in the quotient of blood pressure divided by brachial artery blood velocity. Stimulus–response curves were defined at high altitude (4338 m) and within 1 day of descent to sea level. We applied a sigmoid function or third-order polynomial to the curves and determined the maximal slope (equivalent to peak gain) and the corresponding carotid pressure (equivalent to ‘set point’). The results showed that the peak gains of the reflex were similar in both groups and at both locations. The ‘set point’ of the reflex, however, was significantly higher in the CMS patients compared to HA controls, indicating that the reflex operates over higher pressures in the patients (94.4 ± 3.0 versus 79.6 ± 4.1 mmHg; P < 0.01). This, however, was seen only when subjects were studied at altitude; after descent to sea level the curve reset to a lower pressure with no significant difference between HA and CMS subjects. These results indicate that carotid baroreceptor control of vascular resistance may be abnormal in CMS patients but that descent to sea level rapidly normalizes it. We speculate that this may be explained by CMS patients having greater vasoconstrictor activity at altitude owing to greater hypoxic stimulation of chemoreceptors.

(Received 14 December 2005; accepted after revision 7 June 2006; first published online 8 June 2006)
Corresponding author J. P. Moore: Department of Chemical and Biological Sciences, School of Applied Sciences, University of Huddersfield, Huddersfield HD1 3DH, UK. Email: j.p.moore{at}hud.ac.uk

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