Ceroni Alexandre, Chaar Laiali J, Bombein Rafael L, Michelini Lisete C
Department of Physiology & Biophysics, Institute of Biomedical Sciences, Universidade de São Paulo, São Paulo, SP, Brazil.
Exp Physiol. 2009 Jun;94(6):630-40. doi: 10.1113/expphysiol.2008.046128. Epub 2009 Feb 27.
We investigate whether arterial baroreceptors mediate the training-induced blood pressure fall and resting bradycardia in hypertensive (SHR) and normotensive rats (WKY). Male SHR and WKY rats, submitted to sino-aortic denervation (SAD) or sham surgery (SHAM group), were allocated to training (T; 55% of maximal exercise capacity) or sedentary (S) protocols for 3 months. Rats were instrumented with arterial and venous catheters for haemodynamic measurements at rest (power spectral analysis) and baroreceptor testing. Kidney and skeletal muscles were processed for morphometric analysis of arterioles. Elevated mean arterial pressure (MAP) and heart rate (HR) in SHAM SHRS were accompanied by increased sympathetic variability and arteriolar wall/lumen ratio [+3.4-fold on low-frequency (LF) power and +70%, respectively, versus WKYS, P < 0.05]. Training caused significant HR (approximately 9% in WKY and SHR) and MAP reductions (-8% in the SHR), simultaneously with improvement of baroreceptor reflex control of HR (SHR and WKY), LF reduction (with a positive correlation between LF power and MAP levels in the SHR) and normalization of wall/lumen ratio of the skeletal muscle arterioles (SHR only). In contrast, SAD increased pressure variability in both strains of rats, causing reductions in MAP (-13%) and arteriolar wall/lumen ratio (-35%) only in the SHRS. Training effects were completely blocked by SAD in both strains; in addition, after SAD the resting MAP and HR and the wall/lumen ratio of skeletal muscle arterioles were higher in SHRT versus SHRS and similar to those of SHAM SHRS. The lack of training-induced effects in the chronic absence of baroreceptor inputs strongly suggests that baroreceptor signalling plays a decisive role in driving beneficial training-induced cardiovascular adjustments.
我们研究了动脉压力感受器是否介导了高血压大鼠（SHR）和正常血压大鼠（WKY）训练诱导的血压下降和静息性心动过缓。将接受了主动脉弓去神经支配（SAD）或假手术（假手术组）的雄性SHR和WKY大鼠分为训练组（T；最大运动能力的55%）或久坐组（S），持续3个月。通过动脉和静脉导管对大鼠进行仪器安装，以在静息状态下进行血流动力学测量（功率谱分析）和压力感受器测试。对肾脏和骨骼肌进行处理，以对小动脉进行形态计量分析。假手术SHR大鼠的平均动脉压（MAP）和心率（HR）升高，同时交感神经变异性增加，小动脉壁/腔比值升高（低频（LF）功率增加3.4倍，分别比WKY大鼠增加70%，P<0.05）。训练导致显著的HR降低（WKY和SHR大鼠中约降低9%）和MAP降低（SHR大鼠中降低8%），同时压力感受器对HR的反射控制得到改善（SHR和WKY大鼠），LF降低（SHR大鼠中LF功率与MAP水平呈正相关），骨骼肌小动脉壁/腔比值正常化（仅在SHR大鼠中）。相比之下，SAD增加了两种品系大鼠的压力变异性，仅在SHR大鼠中导致MAP降低（-13%）和小动脉壁/腔比值降低（-35%）。在两种品系中，训练效果均被SAD完全阻断；此外，SAD后，SHR训练组的静息MAP、HR和骨骼肌小动脉壁/腔比值高于SHR假手术组，且与假手术SHR大鼠相似。在长期缺乏压力感受器输入的情况下，缺乏训练诱导的效应强烈表明，压力感受器信号在驱动有益的训练诱导的心血管调节中起决定性作用。
