Action of Atropin and Eserin on Adrenalin Secretion Caused by KGI and CaCL ∗

Abstract

The introduction of CaCl₂ or KC1 into the adrenal circulation is known to cause a secretion of adrenalin (Bacq and Rosenblueth, 1 Feldberg, 2 Katz and Katz 3 ). In the present investigation we have endeavored to determine whether this adrenalin secretion in cats can be influenced by previous injections of atropin or eserin, assuming that atropin may decrease the amount of adrenalin secreted upon CaCl₂ or KC1 injection, while eserin may enhance it. Such results would justify the working-assumption that the salts act on the adrenal medulla by means of an acetylcholin-like transmitter, as has been shown for the action of KC1 on other organs such as salivary glands, tongue, sweat glands (Feldberg and Guimarais 4 ), or for the transmission of splanchnic stimulation to the adrenals (Feldberg and co-workers 5 , 6 ).

Our method of recording the adrenalin output effected by the salts was the one developed by Feldberg and coworkers 7 and used in our previous investigations on CaCl 2 and KC1. 8 It consisted in comparing the effects on blood pressure and nictitating membrane produced by the salt when injected into a vein or into the central stump of the coeliac artery. The animal was eviscerated and with restricted circulation (aorta and vena cava tied at kidney level, the kidney vessels tied close to the kidneys). A small dose of the drug causes little or no effect upon intravenous injections, while the same amount injected into the central end of the coeliac artery reaches the adrenals in more or less concentrated form and may cause an adrenalin secretion. This latter adrenalin secretion manifests itself by a rise in blood pressure and a retraction of the denervated nictitating membrane after some latent period. These effects may be abolished by removal of the adrenals or enhanced by cocaine administration. They persist in decerebrated and pithed animals. Cats under dial anesthesia were used.