J. Koley et al., RECTAL RESPONSE OF CARDIAC ORIGIN IN THE CAT - INVOLVEMENT OF NITRIC-OXIDE AND ACETYLCHOLINE, European journal of pharmacology, 325(2-3), 1997, pp. 181-187
Local application of nicotine over the surface of the left ventricle a
nd also occlusion of the left anterior descending coronary artery in t
he lightly anaesthetised, open-chested, artificially ventilated cat re
sulted a biphasic rectal movement - initial relaxation followed by sus
tained contraction. However, distension of the atrial appendage did no
t evoke any change in rectal motility, indicating the non-involvement
of atrial volume receptors in initiating this rectal response of cardi
ac 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-a
rginine. The contraction phase, however, was abolished by atropine. Fr
om these observations it is clear that the relaxation phase of the rec
tal response to coronary occlusion or epicardial nicotine is mediated
through neither cholinergic nor adrenergic pathways but through the re
lease of nitric oxide whereas the contraction phase of such a cardio-r
ectal response is mediated through the release of the neurotransmitter
, acetylcholine.