Abstract

Long-term interactions between sympathetic and sensory-motor nerves have been shown in several tissues. Previous investigations in this laboratory have demonstrated an increase in cardiac sensory-motor innervation after neonatal sympathectomy by guanethidine and an increase of perivascular sympathetic neurotransmission after neonatal treatment by capsaicin. The present study evaluated the effects of sensory-motor denervation on sympathetic neurotransmission in the heart. Newborn rats were injected with capsaicin or its vehicle (Tween 80). Sympathetic neurotransmission was studied in isolated atria driven at a constant rate (4 Hz) by measuring cardiac responses to electrical field stimulation, in the presence of atropine 1 μM. Inotropism of tyramine, norepinephrine and calcitonin gene-related peptide was also tested. Neonatal capsaicin treatment did not affect cardiac responses to trains of an increasing number (2–32) of field pulses. Moreover, inotropic responses to tyramine did not differ between control, capsaicin- and Tween 80-treated preparations. Neither maximal effect nor pD₂ values were significantly different between the groups. Similarly, the inotropism of calcitonin gene-related peptide was comparable in all groups of atrial preparations. In marked contrast to earlier papers on blood vessels, this study shows a lack of effect of sensory-motor denervation by neonatal capsaicin treatment on cardiac sympathetic neurotransmission. The different neuronal plasticity of vascular and cardiac sensory innervation will be discussed. The present results also indicate that capsaicin-induced sensory-motor denervation is not associated with changes in cardiac responsiveness to calcitonin gene-related peptide.