4.6 Article

Acute hypoxia elicits lasting reductions in the sympathetic action potential transduction of arterial blood pressure in males

期刊

JOURNAL OF PHYSIOLOGY-LONDON
卷 601, 期 3, 页码 669-687

出版社

WILEY
DOI: 10.1113/JP283979

关键词

action potential detection; hypoxia; matched wavelet; muscle sympathetic nerve activity; signal averaging; sympathetic transduction

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Post-hypoxia sympathoexcitation reduces vascular tone and diminishes sympathetic signalling. Blunted sympathetic transduction during acute hypoxia is confirmed, and the effects of hypoxia on the relationship between mean arterial pressure (MAP) and action potential (AP) activity are examined. It is found that MAP changes are blunted during acute hypoxia but restored in recovery, and asynchronous APs elicit smaller MAP changes compared to synchronous APs.
Post-hypoxia sympathoexcitation does not elicit corresponding changes in vascular tone, suggesting diminished sympathetic signalling. Blunted sympathetic transduction following acute hypoxia, however, has not been confirmed and the effects of hypoxia on the sympathetic transduction of mean arterial pressure (MAP) as a function of action potential (AP) activity is unknown. We hypothesized that MAP changes would be blunted during acute hypoxia but restored in recovery and asynchronous APs would elicit smaller MAP changes than synchronous APs. Seven healthy males (age: 24 (3) years; BMI: 25 (3) kg/m(2)) underwent 20 min isocapnic hypoxia (PETO2: 47 (2) mmHg) and 30 min recovery. Multi-unit microneurography (muscle sympathetic nerve activity; MSNA) and continuous wavelet transform with matched mother wavelet was used to detect sympathetic APs during baseline, hypoxia, early (first 7 min) and late (last 7 min) recovery. AP groups were classified as synchronous APs, asynchronous APs (occurring outside an MSNA burst) and no AP activity. Sympathetic transduction of MAP was quantified using signal-averaging, with & UDelta;MAP tracked following AP group cardiac cycles. Following synchronous APs, & UDelta;MAP was reduced in hypoxia (+1.8 (0.9) mmHg) and early recovery (+1.5 (0.7) mmHg) compared with baseline (+3.1 (2.2) mmHg). AP group-by-condition interactions show that at rest asynchronous APs attenuate MAP reductions compared with no AP activity (-0.4 (1.1) vs. -2.2 (1.2) mmHg, respectively), with no difference between AP groups in hypoxia, early or late recovery. Sympathetic transduction of MAP is blunted in hypoxia and early recovery. At rest, asynchronous sympathetic APs contribute to neural regulation of MAP by attenuating nadir pressure responses.

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