혈관 평활근의 수축기전에 관한 연구

• 영문명: Different Mechanisms for the Activation of Vascular Smooth Muscle by Norepinephrine and Depolarization
• 발행기관: 대한생리학회
• 저자명: 홍용우(Hong, Yong-Woo) 고광욱(Ko, Kwang-Wook) 김기환(Kim, Ki-Whan)
• 간행물 정보: 『대한생리학회지』제21권 제2호, 191~200쪽, 전체 10쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 1987.12.30

영문 초록

The activation mechanism of the sustained contractions induced by norepinephrine and K-depolarization was studied in renal vascular muscle. Helical strips of arterial muscle were prepared from rabbit renal arteries. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% O² and kept at 35℃. Renal arterial muscles developed a contracture rapidly when exposed to a 40 mM K-Tyrode solution. In the absence of external Ca²⁺, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with Ca²⁺-antagonist (verapamil) or lanthanum (La³⁺). From these results, it is obvious that K-contracture of renal arterial strip required Ca²⁺ in the medium and this contracture was developed by the increased Ca²⁺-influx due to K-depolarization. Noradrenaline (5 mg/l) induced also a similar sustained contraction rapidly in all strips. Even on the K-contracture and in Ca²⁺-free Tyrode solution and also in the Tyrode solution pretreated with verapamil or La³⁺, noradrenaline produced a contraction. However, the contraction in Ca²⁺-free Tyrode solution was not sustained and decreased gradually. The amplitude of noradrenaline-induced contracture was dependent on external Ca²⁺; The contracture increased dose-dependently, but over 3 mM Ca²⁺, decreased. The results of this experiment suggest that K-contracture was developed by an increased Ca²⁺-influx due to membrane depolarization, while noradrenaline-induced contracture was developed by both transmembrane Ca²⁺-influx and the mobilizaiton of cellular Ca²⁺

키워드

Rabbit renal helical strip Norepinephrine K-contracture Verapamil Lanthanum