Capsaicin-sensitive sensory neurons are involved in the plasma catecholamine response of rats to selective stressors.
1. The effect of capsaicin pre-treatment on adrenal catecholamine (CA) secretion in response to stress is controversial. In earlier experiments performed under pentobarbitone anaesthesia, the release of CA in response to stress was complicated by the effects of the barbiturate anaesthesia. 2. In the present study we have used conscious freely moving rats with indwelling cannulae to study the effect of neonatal capsaicin pre-treatment on the plasma CA response to different types of stressors (swimming stress, hypovolaemic stress, immobilization stress and cold stress). 3. After swimming for 20 min, plasma noradrenaline (NA) levels increased by 8-fold and adrenaline by 2-fold in control rats. The increase in plasma NA levels in the capsaicin group was attenuated at 10 min of swimming compared with the vehicle group (P < 0.05). 4. With hypovolaemic stress, there were no differences in plasma CA levels, blood pressure and heart rate between the capsaicin group and the vehicle group. There were also no differences in plasma CA levels after immobilization stress between the two groups. 5. With cold stress, plasma NA levels increased 5-fold and adrenaline levels by 3-fold over basal at 45 min in the vehicle pre-treated rats. This increase was not observed in the capsaicin group. 6. Immunoreactive substance P was depleted by only 68% in the splanchnic nerve following capsaicin pre-treatment. If the remaining 32% was biologically active substance P then it could account for the maintenance of the response to hypovolaemic and immobilization stress. However, it might be possible that the responses to hypovolaemic and immobilization stresses could be attenuated if a more complete depletion were achieved. 7. These results in conscious rats indicate that capsaicin-sensitive sensory neurons are required for plasma CA response to selective stressors. They are required for CA output in response to cold stress and to the early phase of swimming stress, but not to hypovolaemic stress and immobilization stress.
Zhou
X F
XF
Department of Biochemistry, University of Melbourne, Parkville, Victoria, Australia.
Livett
B G
BG
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002211:Capsaicin / Q000494:pharmacology*; D002395:Catecholamines / Q000097:blood*; D003080:Cold Temperature / Q000009:adverse effects; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D007103:Immobilization / Q000009:adverse effects; D009475:Neurons, Afferent / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D012769:Shock / Q000503:physiopathology; D013312:Stress, Physiological / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D013550:Swimming
D002395:Catecholamines; D002211:Capsaicin; D009638:Norepinephrine; D004837:Epinephrine