Helm J F, Bro S L, Dodds W J, Sarna S K, Hoffmann R G, Arndorfer R C
Department of Medicine, Medical College of Wisconsin, Milwaukee 53226.
Am J Physiol. 1991 Sep;261(3 Pt 1):G377-83. doi: 10.1152/ajpgi.1991.261.3.G377.
We evaluated the control of phasic contractions in opossum esophageal circular smooth muscle by determining the contractile response in vitro to agents that cause membrane depolarization and excitation by different mechanisms. Transverse muscle strips taken from different sites along the length of the smooth muscle esophagus were exposed to progressively increasing concentrations of tetraethylammonium (1-30 mM), K+ (4.6-30 mM), or bethanechol (10(-6) to 10(-2) M). In normally inactive esophageal circular smooth muscle, tetraethylammonium and high K+ concentration elicited phasic contractions that were not blocked by atropine and tetrodotoxin. Bethanechol, an M2 muscarinic receptor agonist that acts selectively on smooth muscle, elicited phasic contractions that were not blocked by tetrodotoxin. We conclude that a latent myogenic oscillatory mechanism for control of phasic contractions exists in esophageal circular smooth muscle and that it may be activated by nonspecific excitation of the smooth muscle membrane. We suggest that this myogenic oscillatory mechanism is likely excited and modulated by nerves.
我们通过测定体外对不同机制引起膜去极化和兴奋的药物的收缩反应，评估了负鼠食管环形平滑肌的相性收缩控制。从食管平滑肌不同长度部位获取的横向肌条，分别暴露于逐渐增加浓度的四乙铵（1 - 30 mM）、K⁺（4.6 - 30 mM）或氨甲酰甲胆碱（10⁻⁶至10⁻² M）中。在正常无活性的食管环形平滑肌中，四乙铵和高浓度K⁺引发的相性收缩不受阿托品和河豚毒素的阻断。氨甲酰甲胆碱是一种选择性作用于平滑肌的M2毒蕈碱受体激动剂，其引发的相性收缩也不受河豚毒素的阻断。我们得出结论，食管环形平滑肌中存在一种潜在的肌源性振荡机制来控制相性收缩，并且它可能通过平滑肌膜的非特异性兴奋而被激活。我们认为这种肌源性振荡机制可能受神经兴奋和调节。
