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首页> 外文期刊>American Journal of Physiology >Reply to 'Letter to the editor: Sympathetically mediated increases in cardiac output, or peripheral vasoconstriction as primary regulator of BP during hyperinsulinemia?'
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Reply to 'Letter to the editor: Sympathetically mediated increases in cardiac output, or peripheral vasoconstriction as primary regulator of BP during hyperinsulinemia?'

机译:Reply to "Letter to the editor: Sympathetically mediated increases in cardiac output, or peripheral vasoconstriction as primary regulator of BP during hyperinsulinemia?"

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reply: We thank Dr. Fadel and colleagues (2) for their complimentary comments and insightful interpretations in regard to our recent article (4), published in the American Journal of Physiology-Heart and Circulatory Physiology. Below we provide our response to the authors' three main points. First, the authors expressed some concern that increases in femoral vascular conductance (FVC) following 5-s pulses of neck suction (NS, -60 Torr) were not observed under basal, noninsulin conditions. Important to this point, we did not expect a fall in sympathetic nervous system activity (SNA) to elicit much vasodilation at baseline in the healthy young adults studied. In fact, the lack of effect of NS on peripheral blood flow in young women agrees with prior work from the Fadel group (1) and others (5). In contrast, an acute reduction of SNA with NS in a cohort of primarily men showed an increase in FVC under basal conditions (3). At first glance, it is logical to deduce that divergent findings could be attributed to differences between young men and women. However, we observed no obvious sex differences in the effect of NS on FVC under basal, noninsulin conditions (main effect of sex, P = 0.651; interaction of sex and NS, P = 0.983). This lack of sex differences was noted in the initial article (4). Most importantly, any apparent lack of an effect of NS on FVC at baseline (when SNA is relatively low) is inconsequential to addressing our main hypothesis, which was that sympathoexcitation evoked by hyperinsulinemia restrains insulin-stimulated peripheral vasodilation and that this would be manifested with the NS maneuver. As displayed in Figs. 1 and 2 of our article (4), it is clear that there is no effect of NS on FVC during hyperinsulinemia despite significant increases in SNA; notably, this observation is not sex specific (interaction of insulin and NS: men, P = 0.929; women, P = 0.980). In contrast, we do observe an effect of NS on cardiac output that is amplified during hyperinsulinemia in both men and women (interaction of insulin and NS: men, P = 0.017; women, P = 0.015). Altogether, these data in young healthy adults cannot be used to support the role of SNA in restraining insulin-induced peripheral vasodilation.

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