Nosál R
Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava.
J Physiol Pharmacol. 1994 Sep;45(3):377-86.
The effect of betaadrenoceptor blocking drugs atenolol and propranolol was studied in both nonstimulated and stimulated isolated rat mast cells. Atenolol did not liberate histamine from non-stimulated mast cells, decreased spontaneous secretion, inhibited 48/80 stimulated histamine release, increased 32P incorporation into membrane phospholipids, decreased membrane fluidisation and decreased arachidonic acid liberation from membrane phospholipids of stimulated mast cells. Propranolol dose-dependently liberated histamine from nonstimulated mast cells and inhibited histamine liberation, it nonsignificantly increased membrane phospholipid turnover but significantly increased membrane fluidisation and inhibited stimulated arachidonic acid liberation in stimulated mast cells. The results indicated the interaction of atenolol and propranolol with mast cell membranes, particularly with the phospholipid bilayer, resulting in a possible inhibition of phospholipase A2 activation. Histamine liberation suggested its displacement from granule binding sites after intracellular propranolol accumulation in mast cells.
在未刺激和刺激的离体大鼠肥大细胞中研究了β肾上腺素能受体阻断药物阿替洛尔和普萘洛尔的作用。阿替洛尔不会从未刺激的肥大细胞中释放组胺，减少自发分泌，抑制48/80刺激的组胺释放，增加32P掺入膜磷脂，降低膜流动性，并减少刺激的肥大细胞膜磷脂中花生四烯酸的释放。普萘洛尔剂量依赖性地从未刺激的肥大细胞中释放组胺并抑制组胺释放，它对膜磷脂周转率的增加不显著，但显著增加膜流动性并抑制刺激的肥大细胞中刺激的花生四烯酸释放。结果表明阿替洛尔和普萘洛尔与肥大细胞膜相互作用，特别是与磷脂双层相互作用，可能导致磷脂酶A2活化受到抑制。组胺释放表明在肥大细胞内普萘洛尔积累后，它从颗粒结合位点被置换出来。
