Krasnikova T L, Hollister A S, Brubaker P
Tsitologiia. 1994;36(1):104-10.
Sodium inhibitory effect on adenylate cyclase activity of human mononuclear lymphocytes was investigated. Adenylate cyclase sensitivity to sodium inhibition was different upon cyclase stimulation with 1-isoproterenol, Gpp(NH)p and NaF. Sodium half-maximum inhibitory doze (ID50) was the smallest for 1-isoproterenol-stimulated adenylate cyclase activity (-40 mM). Cholera toxin did not exert influence on the inhibition of adenylate cyclase by sodium. Ouabain (10-100 microM) increased ID50 by 1.5 fold only for 1-isoproterenol-stimulated cyclase. It was observed that ID50 decreased after a short-term (15 min) 1-isoproterenol activation of intact lymphocytes. It is possible that the smallest sodium ID50 for 1-isoproterenol-stimulated adenylate cyclase is conditioned by sodium interaction with carboxylate residue of aspartate-79 from the cytoplasmic compartment of beta 2-adrenergic receptor (Horstman et al., 1990).
研究了钠对人单核淋巴细胞腺苷酸环化酶活性的抑制作用。在用1-异丙肾上腺素、Gpp(NH)p和NaF刺激环化酶时,腺苷酸环化酶对钠抑制的敏感性不同。钠半数最大抑制剂量(ID50)对于1-异丙肾上腺素刺激的腺苷酸环化酶活性来说最小(-40 mM)。霍乱毒素对钠抑制腺苷酸环化酶没有影响。哇巴因(10 - 100 microM)仅对1-异丙肾上腺素刺激的环化酶使ID50增加了1.5倍。观察到完整淋巴细胞经短期(15分钟)1-异丙肾上腺素激活后ID50降低。1-异丙肾上腺素刺激的腺苷酸环化酶的最小钠ID50可能是由钠与β2-肾上腺素能受体胞质区天冬氨酸-79的羧酸盐残基相互作用所决定的(霍斯特曼等人,1990年)。