Smith J B, Lincoln T M
Am J Physiol. 1987 Jul;253(1 Pt 1):C147-50. doi: 10.1152/ajpcell.1987.253.1.C147.
Atrial natriuretic factor (ANF) produced rapid increases in cyclic GMP (cGMP) in cultured aortic smooth muscle cells. Angiotensin II (ANG II) markedly decreased the accumulation of cGMP that was evoked by ANF. Arginine vasopressin and ATP, which evoke transient increases in free Ca2+ similarly to ANG II, also inhibited cGMP accumulation. The effect of the calcium mobilizing neurohormones was mimicked by the divalent cation ionophore, A23187. The cyclic nucleotide phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, prevented ANG II from inhibiting ANF-evoked cGMP accumulation. ANG II also inhibited cGMP accumulation induced by nitroprusside, a compound that activates cytosolic guanylate cyclase. These findings support the hypothesis that ANG II decreases cGMP accumulation by stimulating cGMP hydrolysis, apparently via a Ca2+-activated cGMP phosphodiesterase.
心房利钠因子（ANF）可使培养的主动脉平滑肌细胞中的环磷酸鸟苷（cGMP）迅速增加。血管紧张素II（ANG II）显著降低了由ANF引起的cGMP积累。精氨酸加压素和ATP与ANG II类似，可引起游离Ca2+的短暂增加，它们也抑制cGMP积累。二价阳离子载体A23187模拟了钙动员神经激素的作用。环核苷酸磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤可阻止ANG II抑制ANF引起的cGMP积累。ANG II还抑制了硝普钠诱导的cGMP积累，硝普钠是一种激活胞质鸟苷酸环化酶的化合物。这些发现支持了这样一种假说，即ANG II通过刺激cGMP水解来降低cGMP积累，显然是通过一种Ca2+激活的cGMP磷酸二酯酶。
