Houslay M D, Bojanic D, Gawler D, O'Hagan S, Wilson A
Biochem J. 1986 Aug 15;238(1):109-13. doi: 10.1042/bj2380109.
The thrombin-stimulated GTPase activity of human platelets was additive with respect to the GTPase stimulation effected by prostaglandin E1, but not with that stimulated by adrenaline, vasopressin and platelet-activating factor (PAF). Treatment of platelet membranes with pertussis toxin partially inhibited the thrombin-stimulated GTPase, but had no effect on the vasopressin-stimulated GTPase activity, whereas cholera toxin treatment had no effect on either of these stimulated GTPase activities. Thrombin, adrenaline and PAF, but not vasopressin, inhibited the adenylate cyclase activity of isolated plasma membranes through the action of Ni only, this being inhibited by pertussis toxin. It is suggested that thrombin exerts effects through both the inhibitory guanine nucleotide regulatory protein Ni and through the putative guanine nucleotide regulatory protein, Np, involved in regulating receptor-stimulated inositol phospholipid metabolism. However, vasopressin appears to exert its effects solely through the putative Np.
人血小板中凝血酶刺激的GTP酶活性与前列腺素E1刺激的GTP酶活性具有加和性,但与肾上腺素、血管加压素和血小板激活因子(PAF)刺激的GTP酶活性不具有加和性。用百日咳毒素处理血小板膜可部分抑制凝血酶刺激的GTP酶,但对血管加压素刺激的GTP酶活性无影响,而霍乱毒素处理对这两种刺激的GTP酶活性均无影响。凝血酶、肾上腺素和PAF(而非血管加压素)仅通过Ni的作用抑制分离的质膜的腺苷酸环化酶活性,此活性被百日咳毒素抑制。提示凝血酶通过抑制性鸟嘌呤核苷酸调节蛋白Ni以及参与调节受体刺激的肌醇磷脂代谢的假定鸟嘌呤核苷酸调节蛋白Np发挥作用。然而,血管加压素似乎仅通过假定的Np发挥作用。