Local application of nicotine over the surface of the left ventricle and also occlusion of the left anterior descending coronary artery in the lightly anaesthetised, open-chested, artificially ventilated cat resulted a biphasic rectal movement--initial relaxation followed by sustained contraction. However, distension of the atrial appendage did not evoke any change in rectal motility, indicating the non-involvement of atrial volume receptors in initiating this rectal response of cardiac origin. The relaxation phase of this response was not abolished by pretreatment with atropine or with phentolamine or propranolol but was abolished by the nitric oxide inhibitor, N(G)-nitro-L-arginine (LNNA), and this blockade of the relaxation phase by LNNA was reversed by L-arginine. The contraction phase, however, was abolished by atropine. From these observations it is clear that the relaxation phase of the rectal response to coronary occlusion or epicardial nicotine is mediated through neither cholinergic nor adrenergic pathways but through the release of nitric oxide whereas the contraction phase of such a cardio-rectal response is mediated through the release of the neurotransmitter, acetylcholine.