Noradrenaline inhibits neurogenic propulsive motor patterns but not neurogenic segmenting haustral progression in the rabbit colon.

Background Excessive sympathetic inhibition may be a cause of colon motor dysfunction. Our aim was to better understand the mechanisms of sympathetic inhibition on colonic motor patterns using the rabbit colon, hypothesizing that noradrenaline selectively inhibits propulsive motor patterns. Methods Changes in motor patterns of the rabbit colon were studied ex vivo using noradrenaline and adrenoceptor antagonists and analyzed using spatiotemporal diameter maps. Key Results Noradrenaline abolished propulsive contractions: it abolished the long-distance contractions (LDCs) from a baseline frequency of 0.8 +/- 0.3 and the clusters of fast propagating contractions (FPCs) at a frequency of 14.4 +/- 2.8 cpm. Both motor patterns recovered after addition of the alpha(2)-adrenoceptor antagonist yohimbine to a frequency of 0.5 +/- 0.2 and 9.9 +/- 3.3 cpm, respectively. The beta-adrenoceptor antagonist propranolol did not prevent the loss of propulsive motor patterns with noradrenaline. Noradrenaline did not inhibit haustral boundary contractions and increased the frequency of the myogenic ripples from 8.3 +/- 1.4 to 10.5 +/- 1.3 cpm which was not affected by yohimbine, propranolol nor the alpha(1)-adrenoceptor blocker prazosin. Conclusions and Inferences Noradrenergic inhibition of propulsive motor patterns is mediated by the alpha(2)-adrenoceptor to inhibit the neurogenic LDCs and the neurogenic clustering of FPCs. The neurogenic haustral boundary contractions are not affected, suggesting that alpha(2-)receptors are on selective neural circuits. The excitatory effect of noradrenaline on ripples may be due to the activation of adrenoceptors on interstitial cells of Cajal, but action on alpha(1-)receptors was excluded. No role for the beta-adrenoceptor was found.