Ruth J A, Cuizon J V, Eiden L E
Biochem Biophys Res Commun. 1983 Dec 16;117(2):536-40. doi: 10.1016/0006-291x(83)91233-0.
Exposure of rat atrial slices to 10(-5) M norepinephrine (NE) for 10 minutes increases 45Ca++ accumulation from 1.64 +/- 0.10 to 2.23 +/- 0.06 nmol/mg tissue. In the presence of leucine enkephalin (10(-8) M), NE-stimulated 45Ca++ uptake is reduced to 1.44 +/- 0.10 nmol/mg tissue. The effect of leu-enkephalin is reversed in the presence of 10(-7) M naloxone, NE-stimulated 45Ca++ uptake being increased to 2.17 +/- 0.15 nmol/mg tissue. The results support a direct interaction of leu enkephalin with beta-agonist-stimulated Ca++ flux in rat atria, and correlate with the previously reported enkephalin antagonism of NE-induced positive chronotropy in the same tissue.
将大鼠心房切片暴露于10⁻⁵M去甲肾上腺素（NE）中10分钟，可使⁴⁵Ca²⁺蓄积量从1.64±0.10增加至2.23±0.06 nmol/mg组织。在亮氨酸脑啡肽（10⁻⁸M）存在的情况下，NE刺激的⁴⁵Ca²⁺摄取量降低至1.44±0.10 nmol/mg组织。在10⁻⁷M纳洛酮存在的情况下，亮氨酸脑啡肽的作用被逆转，NE刺激的⁴⁵Ca²⁺摄取量增加至2.17±0.15 nmol/mg组织。这些结果支持亮氨酸脑啡肽与大鼠心房中β-激动剂刺激的Ca²⁺通量直接相互作用，并且与先前报道的同一组织中脑啡肽对NE诱导的正性变时作用的拮抗作用相关。
