해명 회장 운동에 대한 아드레나린성 α-수용체에 관한 연구

• 영문명: Studies on the Adrenergic Alpha-Receptor in the Guinea Pig Ileum
• 발행기관: 대한약리학회
• 저자명: 고창만(Chang Mann Ko)
• 간행물 정보: 『대한약리학잡지』제19권 제1호, 85~92쪽, 전체 8쪽
• 주제분류: 의약학 > 기타의약학
• 파일형태: PDF
• 발행일자: 1983.06.30

영문 초록

Intestine is innervated by an interconnected plexus of both sympathetic and parasympathetic nerve fibers. Sympathetic influence causes inhibition of intestinal motility mediated by both α- and β-adrenergic receptors. The mechanism of intestinal relaxation by β-receptors has been extensively studied, but the function of α-receptors in intestinal motility is still unclear. Although it is suggested that catecholamine reduces acetylcholine release and this may play an important role in α-receptor mediated intestinal relaxation, there is no definite evidences about the mechanism and site of action of α-receptor mediated relaxation. In this experiment, therefore, the effect and site of action of α-receptor agonists were investigated in the guinea pig ileum using electrical field stimulation. The results are summarized as follows : 1) Electrical field stimulation elicited tonic contraction in isolated guinea pig ileum ana this contraction was completely inhibited by the pretreatment of tetrodotoxin or atropine. 2) Norepinephrine, epinephrine and dopamine inhibited the contraction induced by electrical field stimulation but methoxamine and phenylephrine had little effects. 3) Inhibitory effects of norepinephrine and dopamine was partially blocked by yohimbine and phentolamine pretreatment. But haloperidol and propranolol pretreatment cause no effects on the electrical field stimulation induced contraction. Inhibitory effect of dopamine was completely blocked by both haloperidol and yohimbine pretreatment. 4) Inhibitory effects of norepinephrine and dopamine were little affected by the pretreatment with hexamethonium. It is suggested that electrical field stimulation causes tonic contraction of guinea pig ileum by releasing acetylcholine from postganglionic fiber, and this release is blocked by presynaptic α-receptor activation.