Zavoico G B, Feinstein M B
Biochem Biophys Res Commun. 1984 Apr 30;120(2):579-85. doi: 10.1016/0006-291x(84)91294-4.
Activation of platelets by thrombin rapidly increases cytoplasmic free calcium, [Ca2+]i, measured by Quin -2, and induces secretion. Stimulators of adenylate cyclase (i.e. PGI2, PGD2, forskolin) suppressed or reversed the increase of [Ca2+]i. Inhibitors of adenylate cyclase (i.e. epinephrine, ADP), added before or after thrombin, counteracted PGI2, PGD2 and forskolin and thereby increased [Ca2+]i and restored secretion. Responses to epinephrine (via alpha-2 adrenoreceptors) and ADP were independent of extracellular Ca2+, but required maintained occupancy of thrombin receptors and intact cAMP-phosphodiesterase activity. These results indicate that cAMP serves as an inhibitory second-messenger that antagonizes the mobilization of Ca2+, an activator second-messenger.
凝血酶激活血小板会迅速增加胞质游离钙（[Ca2+]i，通过喹哪啶红 - 2 测量），并诱导分泌。腺苷酸环化酶刺激剂（如前列环素（PGI2）、前列腺素 D2（PGD2）、福斯高林）抑制或逆转了[Ca2+]i 的增加。在凝血酶之前或之后添加的腺苷酸环化酶抑制剂（如肾上腺素、二磷酸腺苷（ADP））会抵消 PGI2、PGD2 和福斯高林的作用，从而增加[Ca2+]i 并恢复分泌。对肾上腺素（通过α - 2 肾上腺素能受体）和 ADP 的反应与细胞外钙无关，但需要凝血酶受体持续被占据以及完整的环磷酸腺苷（cAMP）磷酸二酯酶活性。这些结果表明，cAMP 作为一种抑制性第二信使，拮抗作为激活剂第二信使的 Ca2+ 的动员。
