Sympatho-adrenal stimulation by carbon dioxide and the inhibitory effect of carbonic acid on epinephrine response.

Abstract

Carbon dioxide serves as a potent stimulus to increase the titer of circulating sympatho-adrenal catechol amines in the cat. Using the denervated nictitating membrane as an assay method the CO2 threshold for adrenal stimulus was determined to be about 15% concentration in alvcolar air. Adrenalectomy decreased by 60% the catechol amine titer initiated by 30% CO2, but hepatectomy was ineffective. The stimulant effect of CO2 in this action was specific and was not dependent on the change in hydrogen ion concentration. The spinal cat was almost as responsive as the normal to CO2 stimulus, but if the cord was destroyed only a very low catechol amine concentration could be detected with comparable stimulus. In the intact cat much of the inhibition of response to administered epinephrine by CO2 is more apparent than real, because the CO2 itself serves as a stimulus to raise the endogeneous epinephrine titer and each subsequently administered test dose of epinephrine was then examined against a background of hormone action. Because of the alinear shape of the epinephrine dose-response curve this can be misinterpreted as ‘inhibition.’ There was however, a direct CO2 inhibition of epinephrine-induced smooth muscle contraction which was most apparent in the range 3–15% alveolar CO2. Sympathetically innervated and denervated structures were inhibited to the same degree.