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 ass
essed as changes in mean arterial pressure (MAP) and heart rate (HR). We te
sted the hypothesis that C-type BR inputs are effective at low frequencies
because they outnumber A-type. Anodal current (I-an) reversibly eliminated
all MAP and HR responses to A-selective stimuli. High intensities activated
all ADN axone (A + C) and decreased MAP at lower frequencies (<10 Hz) than
were effective with A-selective stimulation. I-an reduced only MAP respons
es to >10-Hz ADN stimulation. Burst patterns significantly augmented A- but
not C-selective reflex responses despite identical numbers of shocks per s
econd. A-selective stimuli failed to evoke significant bradycardia even at
200 Hz. Maximum intensity stimuli plus I-an (C selective) evoked less brady
cardia than without I-an (A+C), indicating supra-additive summation unlike
the occlusive summation for MAP responses. However, activation of reduced n
umbers of C-type BRs with all A-type BRs suggests a strong A to C interacti
on in reflex bradycardia responses. Surprisingly, I-an block of A-type cond
uction eliminated all reflex bradycardia at such submaximal intensities des
pite C conduction and depressor responses. A- and C-type BRs act synergisti
cally, and A-type activity is absolutely required in cardiac but not in dep
ressor pathways. Thus greater numbers do not appear to account for C-type B
R efficacy, and critical interactions between these two sensory subtypes ap
pear to occur differentially across cardiac and systemic baroreflex effecto
r pathways.