Reflex activation of the adrenal medulla during hypoglycemia and circulatory dysregulations is regulated by capsaicin-sensitive afferents.

1. Catecholamines were measured in the adrenal venous outflow during hypoglycemia, hypotension, hypovolaemia and efferent splanchnic nerve stimulation in anaesthetized capsaicin-pretreated rats and their vehicle controls. In control rats, efferent splanchnic nerve stimulation caused a marked rise in adrenaline and noradrenaline levels. In contrast, the other stimuli mainly elicited adrenaline release. 2. The release of adrenaline and nor-adrenaline evoked by splanchnic nerve stimulation was of the same magnitude in capsaicin-pretreated rats (whose afferent C-fibres were destroyed by this pretreatment) as in their untreated controls. 3. Capsaicin-pretreatment of rats resulted, however, in a reduced adrenaline release during insulin-induced hypoglycemia for up to 30 min and, as a consequence, generated a greater fall in blood glucose. The adrenal response to hypoglycemia in the first 30 min was also reduced by bilateral vagotomy indicating the existence of glucoreceptors on peripheral vagal terminals. 4. Adrenaline secretion following central glucopenia induced by 2-deoxy-D-glucose remained unaffected by capsaicin-pretreatment, indicating an intact function of the central regulation of adrenaline release. 5. Hypotension evoked either by sodium nitroprusside or by haemorrhage resulted in a pronounced increase in adrenaline release which was almost absent in the capsaicin-pretreated rats. 6. It is concluded that the stimulation of the adrenal medulla during hypoglycemia, hypotension, and hypovolaemia is based on a reflex mechanism initiated by capsaicin sensitive afferents.