2型糖尿病(T2D)常伴有高血压,过度的血压(BP)对交感神经兴奋性应激源的反应,增加了心血管疾病的风险。适当的呼吸-交感神经耦合和交感神经传导对BP的短期和长期BP控制很重要。我们测试了以下假设:在T2D中,肌肉交感神经活动(MSNA)的呼吸调节及其对BP的转导将受到损害,并与较高的BP和呼吸耦合BP变异性相关。静息MSNA,记录了20名T2D(49.1±7.4年;平均值±SD)和13名健康对照(46.3±9.4年)参与者的呼吸和逐搏BP。在低肺容量和高肺容量阶段比较了MSNA和交感神经爆发(信号平均)对平均动脉压(MAP)的转导。在高肺容量阶段,交感神经爆发后的峰值MAP反应低于对照组的低肺容量阶段(P=0.005),而T2D参与者的相位不变(P=0.522)。在T2D参与者中,MSNA的呼吸调节受损,从低肺容量到高肺容量阶段,爆发发生率的降低有所减弱,与对照组(27.8±38.4%vs.49.4±24.6%,分别;P=0.043)。将T2D参与者分为未受损的呼吸调节剂(突发发生率调制中位数或以上)或受损的呼吸调节剂(低于中位数)。受损的调节剂有较高的收缩压(133±14vs.121±11mmHg,P=0.046),更大的Traube-Hering波振幅(6.3±2.4与4.6±1.1mmHg;P=0.028)和更高的BP变异性(MAP平均实际变异性,2.0±0.7vs.1.4±0.3,P=0.033)。在T2D患者中,MSNA的呼吸调节和交感神经对BP的传导发生了改变,并可能导致高血压和心血管风险增加。关键点:呼吸-交感神经耦合和交感神经传导对血压(BP)的影响有助于短期和长期BP控制。我们对健康和2型糖尿病(T2D)中这些过程的理解,高血压和心血管风险高的情况,是不完整的。我们发现,在健康个体中,呼吸和交感神经对BP的传导是耦合的。与低肺容量阶段相比,在高肺容量阶段,对交感神经爆发的平均动脉压反应降低。这种偶联在T2D中不存在。在T2D中,肌肉交感神经活动(MSNA)的呼吸调制受损,在高肺容量阶段观察到MSNA的减弱。呼吸MSNA调节受损的T2D患者收缩压增加,与呼吸相关的BP偏移(Traube-Hering波)和BP变异性。T2D中MSNA的异常呼吸调节和交感神经向BP的转导可能导致该人群的血压控制和心血管风险改变。
Type 2 diabetes (T2D) is often accompanied by hypertension, exaggerated blood pressure (BP) responses to sympatho-excitatory stressors, and raised cardiovascular disease risk. Appropriate respiratory-sympathetic coupling and sympathetic
transduction to BP are important for short- and longer-term BP control. We tested the hypotheses that respiratory modulation of muscle sympathetic nerve activity (MSNA) and its
transduction to BP would be impaired in T2D and associated with higher BP and respiratory-coupled BP variability. Resting MSNA, respiration and beat-to-beat BP were recorded in 20 T2D (49.1 ± 7.4 years; mean ± SD) and 13 healthy control (46.3 ± 9.4 years) participants. MSNA and the
transduction of sympathetic bursts (signal-averaging) to mean arterial pressure (MAP) were compared at low and high lung volume phases. The peak MAP response following a sympathetic burst was lower during the high lung volume than low lung volume phase in controls (P = 0.005), whereas it was unchanged with phase in T2D participants (P = 0.522). Respiratory modulation of MSNA was impaired in T2D participants, who had an attenuated reduction in burst incidence from low to the high lung volume phase, versus controls (27.8 ± 38.4% vs. 49.4 ± 24.6%, respectively; P = 0.043). The T2D participants were grouped into unimpaired respiratory modulators (burst incidence modulation median or above) or impaired respiratory modulators (below median). Impaired modulators had higher systolic BP (133 ± 14 vs. 121 ± 11 mmHg, P = 0.046), greater Traube-Hering wave amplitudes (6.3 ± 2.4 vs. 4.6 ± 1.1 mmHg; P = 0.028) and higher BP variability (MAP average real variability, 2.0 ± 0.7 vs. 1.4 ± 0.3, P = 0.033). Respiratory modulation of MSNA and sympathetic
transduction to BP are altered in T2D patients and may contribute to their increased hypertension and cardiovascular risk. KEY POINTS: Respiratory-sympathetic coupling and sympathetic transduction to blood pressure (BP) contribute to short- and longer-term BP control. Our understanding of these processes in health and type 2 diabetes (T2D), a condition with high prevalence of hypertension and cardiovascular risk, is incomplete. We found that respiration and sympathetic
transduction to BP are coupled in healthy individuals. The mean arterial pressure response to a sympathetic burst was reduced during the high lung volume compared to the low lung volume phase. This coupling was absent in T2D. Respiratory modulation of muscle sympathetic nerve activity (MSNA) is impaired in T2D, with a blunted reduction of MSNA observed during the high lung volume phase. T2D patients with impaired respiratory MSNA modulation had augmented systolic BP, respiratory-related BP excursions (Traube-Hering waves) and BP variability. Abnormal respiratory modulation of MSNA and sympathetic transduction to BP in T2D may contribute to altered blood pressure control and cardiovascular risk in this population.