Influence of adrenergic and cholinergic mediators on the equine jejunum in vitro.
OBJECTIVE
To characterize the response of equine jejunal smooth muscle to adrenergic and cholinergic mediators.


METHODS
Evaluation of myogenic responses, using an in vitro model.


METHODS
Intestinal tissues were obtained from horses without gastrointestinal tract disorders or systemic disease.


METHODS
Baseline myogenic tone and amplitude and frequency of contraction were determined for suspended jejunal muscle strips. The level of adrenergic and cholinergic regulation was assessed, using atropine and adrenoceptor antagonists. The response of the muscles to norepinephrine was characterized, using adrenergic blockade and alpha- and beta-agonists.


RESULTS
Adrenergic and cholinergic blockade had minimal effect on baseline myogenic activity. However, alpha 1- and beta 2-agonists induced significant (P < 0.05) decreases in the amplitude and frequency of contraction. Surprisingly, alpha 2-agonists caused an increase in the contraction amplitude of longitudinal muscle fibers (neurogenic in origin). Change in circular muscle activity was not induced by alpha 2-agonists. Norepinephrine induced a similar selective response and was inhibited by yohimbine.


CONCLUSIONS
Baseline jejunal activity appears to be myogenic in origin and can function independently of sympathetic and parasympathetic input. However, intestinal smooth muscle can be affected by adrenergic agonists and potentially by increased concentrations of circulating catecholamines. Norepinephrine may act by altering the activity of other neurotransmitters. Differing responses between circular and longitudinal muscle fibers indicates a need to evaluate both components.


CONCLUSIONS
Selective alpha 2-agonists may be potentially useful for motility modification of the equine jejunum. Therapeutic use of adrenergic blockade will be effective only in cases of increased adrenergic stimulation.
Malone
E D
ED
Department of Clinical and Population Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul 55108, USA.
Brown
D R
DR
Trent
A M
AM
Turner
T A
TA
D000109:Acetylcholine / Q000494:pharmacology; D000322:Adrenergic Agonists / Q000494:pharmacology*; D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D000068438:Brimonidine Tartrate; D002121:Calcium Channel Blockers / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology*; D018680:Cholinergic Antagonists / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006736:Horses / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D007583:Jejunum / Q000187:drug effects* / Q000294:innervation / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010109:Oxymetazoline / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D002121:Calcium Channel Blockers; D018679:Cholinergic Agonists; D018680:Cholinergic Antagonists; D011810:Quinoxalines; D010656:Phenylephrine; D015016:Yohimbine; D013779:Tetrodotoxin; D000068438:Brimonidine Tartrate; D001285:Atropine; D010109:Oxymetazoline; D014700:Verapamil; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine; D011224:Prazosin; D010646:Phentolamine