Fan W, Schild J H, Andresen M C
Department of Physiology and Pharmacology, Oregon Health Sciences University, Portland, Oregon 97201-3098, USA.
Am J Physiol. 1999 Sep;277(3):R748-56. doi: 10.1152/ajpregu.1999.277.3.R748.
Unmyelinated (C) and myelinated (A) baroreceptor (BR) axons are present in rat aortic depressor nerve (ADN). With graded ADN electrical activation and anodal conduction blockade, reflex responses in anesthetized rats were assessed as changes in mean arterial pressure (MAP) and heart rate (HR). We tested the hypothesis that C-type BR inputs are effective at low frequencies because they outnumber A-type. Anodal current (Ian) reversibly eliminated all MAP and HR responses to A-selective stimuli. High intensities activated all ADN axons (A+C) and decreased MAP at lower frequencies (<10 Hz) than were effective with A-selective stimulation. I(an) reduced only MAP responses to >10-Hz ADN stimulation. Burst patterns significantly augmented A- but not C-selective reflex responses despite identical numbers of shocks per second. A-selective stimuli failed to evoke significant bradycardia even at 200 Hz. Maximum intensity stimuli plus Ian (C selective) evoked less bradycardia than without I(an) (A+C), indicating supra-additive summation unlike the occlusive summation for MAP responses. However, activation of reduced numbers of C-type BRs with all A-type BRs suggests a strong A to C interaction in reflex bradycardia responses. Surprisingly, Ian block of A-type conduction eliminated all reflex bradycardia at such submaximal intensities despite C conduction and depressor responses. A- and C-type BRs act synergistically, and A-type activity is absolutely required in cardiac but not in depressor pathways. Thus greater numbers do not appear to account for C-type BR efficacy, and critical interactions between these two sensory subtypes appear to occur differentially across cardiac and systemic baroreflex effector pathways.
大鼠主动脉减压神经（ADN）中存在无髓鞘（C类）和有髓鞘（A类）压力感受器（BR）轴突。通过对ADN进行分级电刺激和阳极传导阻滞，以平均动脉压（MAP）和心率（HR）的变化来评估麻醉大鼠的反射反应。我们检验了这样一个假设，即C类BR输入在低频时有效是因为它们的数量超过A类。阳极电流（Ian）可可逆地消除所有对A类选择性刺激的MAP和HR反应。高强度刺激激活了所有ADN轴突（A + C），并且在比A类选择性刺激更低的频率（<10 Hz）下降低了MAP。Ian仅降低了对>10 Hz的ADN刺激的MAP反应。尽管每秒的电击次数相同，但爆发模式显著增强了A类而非C类选择性反射反应。即使在200 Hz时，A类选择性刺激也未能引起明显的心动过缓。最大强度刺激加上Ian（C类选择性）引起的心动过缓比不使用Ian（A + C）时少，这表明与MAP反应的阻塞性总和不同，存在超相加总和。然而，激活减少数量的C类BR与所有A类BR表明在反射性心动过缓反应中A类与C类之间存在强烈的相互作用。令人惊讶的是，尽管存在C类传导和降压反应，但在这种次最大强度下，Ian对A类传导的阻滞消除了所有反射性心动过缓。A类和C类BR协同作用，并且在心脏反射途径中绝对需要A类活动，但在降压途径中则不需要。因此，数量更多似乎并不能解释C类BR的功效，并且这两种感觉亚型之间的关键相互作用似乎在心脏和全身压力反射效应途径中存在差异。
