Weglicki W B, Kramer J H, Kennett F F, Knauer T E, Owens K
Adv Myocardiol. 1985;6:127-36.
Sarcolemmal (SL) and microsomal (MC) membranes were prepared from adult canine cardiocytes. SL Na+, K+-ATPase (2.35 mumole/min per mg) was enriched 117-fold over the homogenate and MC rotenone-insensitive NADH cytochrome c reductase (RINCR) was enriched 41-fold. Preincubation of SL with 50 microM arachidonyl-CoA (20:4 CoA) stimulated Na+, K+-ATPase almost 2-fold; 250 microM 20:4 CoA inhibited the enzyme by 85%. However, RINCR was inhibited 80% by only 0.2 microM 20:4 CoA. Thus, each of these myocardial lipid-dependent enzymes showed a different sensitivity to perturbation by lipid amphiphiles. In further experiments, SL preincubated with 50 microM 20:4 CoA + 2.5 mM propranolol (which had no effect alone) exhibited a synergistic inhibition of the Na+, K+-ATPase: The enzymatic activity declined 8.5-fold when compared to sarcolemma treated with 50 microM 20:4 CoA alone. Thus, the presence of lipid amphiphiles may result in greater inhibition of the Na+, K+-ATPase when propranolol is present in the membrane.
从成年犬心肌细胞制备肌膜（SL）和微粒体（MC）膜。SL的Na⁺，K⁺-ATP酶（2.35微摩尔/分钟/毫克）比匀浆富集了117倍，MC的鱼藤酮不敏感的NADH细胞色素c还原酶（RINCR）富集了41倍。用50微摩尔花生四烯酰辅酶A（20:4 CoA）预孵育SL可使Na⁺，K⁺-ATP酶活性几乎提高2倍；250微摩尔20:4 CoA可使该酶活性抑制85%。然而，仅0.2微摩尔20:4 CoA就能使RINCR抑制80%。因此，这些心肌脂质依赖性酶中的每一种对脂质两亲物的扰动都表现出不同的敏感性。在进一步的实验中，用50微摩尔20:4 CoA + 2.5毫摩尔普萘洛尔（单独使用无作用）预孵育的SL对Na⁺，K⁺-ATP酶表现出协同抑制作用：与仅用50微摩尔20:4 CoA处理的肌膜相比，酶活性下降了8.5倍。因此，当膜中存在普萘洛尔时，脂质两亲物的存在可能会导致对Na⁺，K⁺-ATP酶的更大抑制。
