Sympathetic neurotransmission in isolated rat atria after sensory-motor denervation by neonatal treatment with capsaicin

Rubino, A.; Ralevic, V.; Burnstock, G.

Journal of Pharmacology and Experimental Therapeutics 282(2): 671-675

1997


ISSN/ISBN: 0022-3565
PMID: 9262329
Document Number: 474742
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 microM. 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.

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