Modulation of the prostaglandin-induced intestinal motility in humans through the transmitters of the vegetative nervous system.
Research was done on the reciprocity between adrenergic and cholinergic stimulating or inhibiting pharmaceuticals and the prostaglandin-induced intestinal motility. By cholinergic activation, the amplitudes of the prostaglandin-dependent rhythmical contractions of human taenia coli were intensified. There was very little influence on the frequency of contractions, however. Simultaneous stimulation of adrenergic beta-receptors by increasing doses of adrenaline or noradrenaline caused the contraction amplitude and frequency to decrease continually until the contractions were completely eliminated. The cholinergic effect could be suppressed with atropine, the adrenergic-stimulated reaction was reversed by the blockage of beta-receptors. It was completely abolished by simultaneous addition of alpha- and beta-receptor-blocking drugs.
D000109:Acetylcholine / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D003106:Colon / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology; D005769:Gastrointestinal Motility / Q000187:drug effects*; D006801:Humans; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D011941:Receptors, Adrenergic / Q000187:drug effects*; D011950:Receptors, Cholinergic / Q000187:drug effects*
D011458:Prostaglandins E; D011460:Prostaglandins F; D011941:Receptors, Adrenergic; D011950:Receptors, Cholinergic; D001285:Atropine; D002217:Carbachol; D000109:Acetylcholine; D009638:Norepinephrine; D004837:Epinephrine