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Carotid baroreflex regulation of vascular resistance in high‐altitude Andean natives with and without chronic mountain sickness
Author(s) -
Moore Jonathan P.,
Claydon Victoria E.,
Norcliffe Lucy J.,
RiveraCh Maria C.,
LèonVelarde Fabiola,
Appenzeller Otto,
Hainsworth Roger
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2005.033084
Subject(s) - baroreceptor , baroreflex , medicine , vascular resistance , cardiology , blood pressure , reflex , effects of high altitude on humans , brachial artery , anesthesia , hemodynamics , heart rate , anatomy
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.