Contractor responses of the isolated colon of the mouse to morphine and some opioid peptides.

Morphine (1 X 10(-8) - 1 X 10(-4)M), fentanyl (1 X 10(-9) - 1 X 10(-5)M) and alfentanyl (1 X 10(-10) - 1 X 10(-5)M) as well as methionine enkephalin [Met5]enkephalin (1 X 10(-11) - 1 X 10(-8)M), [D-Ala2, Met5]enkephalin (1 X 10(-12) - 1 X 10(-8)M) and dynorphin A(1 - 13) (1 X 10(-9) - 1 X 10(-6)M) caused a contractor response of the longitudinal musculature of the terminal colon of the mouse. These effects were competitively antagonized by naloxone. The pA2 values obtained for naloxone antagonism of morphine and opioid peptides and the high sensitivity of the preparation to enkephalins suggest the presence of delta-opiate receptors in this preparation but mu- and kappa-receptors may also be present. Opiate-induced contractions in the mouse colon were abolished by tetrodotoxin and after incubation with indomethacin. It is concluded that the excitatory actions of the opiates in the mouse colon are mediated via opiate receptors located on nerves which do not release acetylcholine, noradrenaline or 5-hydroxytryptamine. The opiates may produce their action by removing an inhibitory neural influence (the nature of which remains to be elucidated) allowing a prostaglandin-mediated effect to predominate, thereby increasing muscle tone.