Response by Holwerda et al to Letter Regarding Article "Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults".
Response by Holwerda et al to Letter Regarding Article "Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults".
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Holwerda 等人对有关文章“肌肉交感神经活动升高导致年轻和中年/老年人中央动脉僵硬”的信件的回应。
DOI：
10.1161/hypertensionaha.119.13299
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Pierce,GaryL
中科院分区：
文献类型：
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作者：
Holwerda,SethW;Fadel,PaulJ;Abboud,FrancoisM;Pierce,GaryL
We read the letter by Mäki-Petäjä et al1 and address some major discrepancies and misrepresentations in their arguments. The major argument in their letter is that lower body negative pressure (LBNP) increases aortic stiffness not because of elevated sympathetic nerve activity (SNA), but instead dilation of the aorta resulting from greater transmural pressure across the aortic wall. However, there are no data in humans to indicate that LBNP reduces intraabdominal pressure sufficiently and uniformly to increase aortic transmural pressure and diameter. Most importantly, the study by Sonesson et al, 2 which is cited in support of their contention, demonstrated convincingly that lower abdominal aortic diameter does not change during LBNP even at negative pressures greater than those used in our study, thus directly refuting their argument. In addition, Mäki-Petäjä et al1 have disregarded key data from our study demonstrating increased carotid-brachial pulse wave velocity and reduced carotid artery compliance during LBNP. These are important findings because the brachial and carotid arteries were not in the LBNP chamber and therefore not subject to the suction effect that Mäki-Petäjä et al1 suggest explains the increase in arterial stiffness. To further support their contention that SNA does not contribute to aortic stiffness, Mäki-Petäjä et al1 cite their work and others3 that did not make direct measurements of SNA. Conclusions were based on heart rate variability, which is an indirect assessment of parasympathetic as well as sympathetic regulation of heart rate, rather than SNA to the peripheral or central vasculature. Therefore, the relation between SNA and aortic stiffness was not accurately assessed. Another important reason why the interpretation of the results of the study by Mäki-Petäjä et al1 is flawed is because PWV was assessed during experimental maneuvers (ganglionic blockade and static handgrip) that acutely altered distending pressure, that is, blood pressure, which is a major determining factor of the mechanical properties of the vessel. The authors relied on a statistical adjustment to fix the inadvertent changes in mechanical properties of the aorta resulting from acute changes in distending pressure in a small sample of healthy young subjects. 1 In contrast, the methodology used in our study4 was rigorous and overcame these above-mentioned limitations. Finally, the statement made in their letter that the association between muscle SNA and aortic stiffness did not remain significant after adjusting for age and blood pressure is incorrect. In our study, the association remained significant after adjusting for blood pressure. Indeed, the association was attenuated only with the addition of age. It was not surprising that an association between muscle SNA and PWV would be weakened in a statistical model including age because it is well-known that these 2 physiological variables (muscle SNA and PWV) rise with advancing age, and therefore statistically adjusting for age would likely abolish the relation. For this very reason, we studied young and middle-age/older adults using LBNP to directly manipulate muscle SNA as discussed above. Accordingly, our study design was comprehensive and the title of the article, the discussion and the accompanying editorial are not misrepresentative because they reflect the entire data set.
