Abstract-Caerulein produces an acceleration of motility of rabbit ileum (in situ). The effect appears to be based on peripheral action. Sympathetic nerve endings appear not to be involved in the action. In the small intestine transit test (mouse) caerulein accelerated the transit when carbon powder was present. It is therefore considered that caerulein does not induce generalized muscle contraction but rather a coordinated propulsion in the intestinal tract. Caerulein in a larger dose discontinues flow of content out of the stomach probably due to pyloric spasm. Caerulein produced contraction of rabbit gallbladder (in situ) at doses lower than the threshold dose of ileum motility acceleration. In isolated ileum of guinea-pig, caerulein produced contraction at low doses. The action of caerulein appears to be mediated through the nerve: it appears to act on non-nicotinic receptor of the cholinergic nervous element and accelerate liberation of acetylcholine. It also appears to act, at least in part, on the atropine-resistant nervous element. In isolated guinea-pig gallbladder, as different from the in situ case, caerulein produced contraction at doses almost equal to the threshold of contraction in isolated guinea-pig ileum. The action of caerulein appears to be a direct action on the gallbladder smooth muscle. Caerulein had no effect on isolated was deferens and uterus. For this reason, the action of caerulein is considered to be of organ specificity.Caerulein is a decapeptide which was extracted from the skin of Australian Hyla caerulea by Anastasi, Erspamer and Endean in 1967 (1). Amino acid composition and sequence of caerulein are shown in the following structure.Chemical structures