기니픽 심장과 심근 세포에서 α1-Adrenergic 자극에 의한 Mg2⁢ 유리조절

• 영문명: Regulation of Mg^2⁢ Release in Guinea Pig Heart and Isolated Ventricular Myocytes by Ձ₁-Adrenergic Stimulation
• 발행기관: 대한생리학회-대한약리학회
• 저자명: 강형섭(Hyung Sub Kang) 장성은(Sung Eun Chang) 김진상(Jin Sang Kim)
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제1권 제6호, 717~730쪽, 전체 14쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 1997.01.01

영문 초록

Mg^2⁢ is the fourth most abundant cation in cellular organisms. Although the biological chemistry and the physiological roles of the magnesium ion were well known, the regulation of intracellular Mg^2⁢ in mammalian cells is not fully understood. More recently, however, the mechanism of Mg^2⁢ mobilization by hormonal stimulation has been investigated in hearts and in myocytes. In this work we have investigated the regulation mechanism responsible for the Mg^2⁢ mobilization induced by α₁-adrenoceptor stimulation in perfused guinea pig hearts or isolated myocytes. The Mg^2⁢ content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry.

The elimination of Mg^2⁢ in the medium increased the force of contraction of right ventricular papillary muscles. Phenylephrine also enhanced the force of contraction in the presence of Mg^2⁢-free medium. α₁-Agonists such as phenylephrine were found to induce Mg^2⁢ efflux in both perfused hearts or myocytes. This was blocked by prazosin, a α₁-adrenoceptor antagonist. Mg^2⁢ efflux by phenylephrine was amplified by Na^⁢ channel blockers, an increase in extracellular Ca^2⁢ or a decrease in extracellular Na^⁢. By contrast, the Mg^2⁢ influx was induced by verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused hearts, but not in myocytes. W₇, a Ca^2⁢/calmodulin antagonist, completely blocked the pheylephrine-, A23187-, veratridine-, Ca^2⁢-induced Mg^2⁢ efflux in perfused hearts or isolated myocytes. In addition, Mg^2⁢ efflux was induced by W₇ in myocytes but not in perfused heart.

In conclusion, An increase in Mg^2⁢ efflux by α₁-adrenoceptor stimulation in hearts can be through IP₃ and Ca^2⁢-calmodulin dependent mechanism.

키워드

α₁-adrenoceptor Magnesium Cardiac myocytes Phenylephrine Heart