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pubmed:abstractText |
We have previously shown that activation of peripheral chemoreceptors with isocapnic hypoxia resets arterial baroreflex control of heart rate and sympathetic vasoconstrictor outflow to higher pressures, without changes in baroreflex gain. We tested the hypothesis that activation of central chemoreceptors with mild hyperoxic hypercapnia also causes resetting of the arterial baroreflex, but that this resetting would not occur with matched volume and frequency hyperpnoea. Baroreflex control of heart rate (n = 16) and muscle sympathetic nerve activity (microneurography; n = 11) was assessed in healthy men and women, age 20-33 years, using the modified Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above eucapnia). Baroreflex trials were separated by 30 min of rest. While neither hyperpnoea nor hypercapnia changed mean arterial pressure (92.0 +/- 1.8 during eucapnia versus 91.0 +/- 1.2 and 90.7 +/- 1.4 mmHg during hyperpnoea and hypercapnia; P = 0.427) or muscle sympathetic nerve activity (2,301 +/- 687 during eucapnia versus 2,959 +/- 987 and 2,272 +/- 414 total integrated units min(-1) during hyperpnoea and hypercapnia; P = 0.653), heart rate was increased from 59.3 +/- 2.7 during eucapnia to 63.2 +/- 3.0 and 62.4 +/- 2.8 beats min(-1) during hyperpnoea and hypercapnia (both P < 0.017). Baroreflex gain was not altered by hyperpnoea or hypercapnia. Thus, acute activation of central chemoreceptors with mild hyperoxic hypercapnia does not affect arterial pressure, sympathetic vasoconstrictor outflow, or baroreflex gain. Heart rate is elevated during hyperoxic hypercapnia, but this response is not different from the increase in heart rate produced by matched volume and frequency hyperpnoea. Therefore, mild activation of central chemoreceptors does not appear to alter arterial baroreflex function.
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