期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 322, 期 6, 页码 R620-R628出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00034.2022
关键词
blood pressure; lower body negative pressure; muscle sympathetic nerve activity; sympathetic transduction
类别
资金
- Natural Science and Engineering Research Council of Canada (NSERC) Discovery Grant program
- Canada Foundation for Innovation
- Ontario Ministry of Research, Innovation and Science
- American Physiological Society Arthur C. Guyton Award for Excellence in Integrative Physiology
- Ontario Ministry of Economic Development, Job Creation and Trade
- Canadian Institute of Health Research (CIHR) Frederick Banting and Charles Best Canada Graduate Scholarship
The sympathetic transduction of blood pressure is negatively correlated with resting muscle sympathetic nerve activity. The acute effects of increasing sympathetic nerve activity on blood pressure are still unclear. This study used lower body negative pressure to increase sympathetic nerve activity and found that it did not alter the traditional measures of sympathetic transduction of blood pressure. Further research is needed to determine the factors that affect the firing of sympathetic nerve activity in relation to blood pressure oscillations.
Sympathetic transduction of blood pressure (BP) is correlated negatively with resting muscle sympathetic nerve activity (MSNA) in crosssectional data, but the acute effects of increasing MSNA are unclear. Sixteen (4 female) healthy adults (26??3 years) underwent continuous measurement of heart rate, BP, and MSNA at rest and during graded lower body negative pressure (LBNP) at -10, -20, and -30 mmHg. Sympathetic transduction of BP was quantified in the time (signal averaging) and frequency (MSNA-BP gain) domains. The proportions of MSNA bursts firing within each tertile of BP were calculated. As expected, LBNP increased MSNA burst frequency (P < 0.01) and burst amplitude (P 0.02), although the proportions of MSNA bursts firing across each BP tertile remained stable (all P 0.44). The MSNA-diastolic BP low-frequency transfer function gain (P = 0.25) was unchanged during LBNP; the spectral coherence was increased (P = 0.03). Signal-averaged sympathetic transduction of diastolic BP was unchanged (from 2.1??1.0 at rest to 2.4?? 1.5, 2.2?? 1.3, and 2.3??1.4 mmHg; P = 0.43) during LBNP, but diastolic BP responses following nonburst cardiac cycles progressively decreased (from-0.8 ?? 0.4 at rest to -1.0 ?? 0.6, -1.2 ?? 0.6, and -1.6 ?? 0.9 mmHg; P < 0.01). As a result, the difference between MSNA burst and nonburst diastolic BP responses was increased (from 2.9??1.4 at rest to 3.4?? 1.9, 3.4?? 1.9, and 3.9??2.1 mmHg; P < 0.01). In conclusion, acute increases in MSNA using LBNP did not alter traditional signal-averaged or frequency-domain measures of sympathetic transduction of BP or the proportion of MSNA bursts firing at different BP levels. The factors that determine changes in the firing of MSNA bursts relative to oscillations in BP require further investigation.
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