Seleznev Iu M, Martynov A V, Smirnov V N
Biull Eksp Biol Med. 1982 May;93(5):72-4.
In vivo administration of propranolol considerably inhibits the isoproterenol-stimulated increase in 45Ca accumulation by the myocardium and completely eliminates the potentiation of isoproterenol effect by hydrocortisone. A significant lowering of the concentration of high affinity binding sites for calcium in the sarcolemmal membranes can be produced by propranolol in vitro. Under these conditions, the glucocorticoids do not change the sarcolemmal Ca2+-binding parameters or modulate the propranolol effect. Therefore, for the manifestation of glucocorticoid action to be brought about, the integrity of the cells is apparently required, while propranolol seems to change calcium binding by direct interaction with the sarcolemmal membranes. It is suggested that in vivo propranolol inhibition of catecholamine effect on calcium ion accumulation by the myocardium depends on the interaction with the beta-receptors and direct modulation of the concentration of high affinity binding sites for calcium ions on the surface of the sarcolemma.
体内给予普萘洛尔可显著抑制异丙肾上腺素刺激引起的心肌45Ca蓄积增加，并完全消除氢化可的松对异丙肾上腺素作用的增强效应。普萘洛尔在体外可使肌膜中钙高亲和力结合位点的浓度显著降低。在这些条件下，糖皮质激素不会改变肌膜Ca2+结合参数，也不会调节普萘洛尔的作用。因此，糖皮质激素作用的表现显然需要细胞的完整性，而普萘洛尔似乎通过与肌膜直接相互作用来改变钙结合。提示体内普萘洛尔抑制儿茶酚胺对心肌钙离子蓄积的作用，依赖于与β受体的相互作用以及对肌膜表面钙离子高亲和力结合位点浓度的直接调节。
