Ishida A, Tanahashi T, Okumura K, Hashimoto H, Ito T, Ogawa K, Satake T
Second Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Life Sci. 1988;42(17):1659-67. doi: 10.1016/0024-3205(88)90445-6.
The role of intracellular signals in the regulation of atrial natriuretic peptide (ANP) release was investigated using isolated rat left atria. Dibutyryl cyclic AMP and dibutyryl cyclic GMP had no effect on ANP release. Arginine vasopressin and phenylephrine, both of which activate the polyphosphoinositide system and consequently both the diacylglycerol-protein kinase C system and the Ca2+-Ca2+ receptor system, stimulated ANP release dose-dependently. The ANP release stimulated by phenylephrine was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin antagonist, and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a protein kinase C inhibitor. Atrial stretch stimulated ANP release, but the release was not inhibited by W-7 or H-7. These results suggest that the mechanism responsible for phenylephrine-induced ANP release differs from that for stretch-induced ANP release.
利用离体大鼠左心房研究了细胞内信号在心房钠尿肽（ANP）释放调节中的作用。二丁酰环磷酸腺苷（dibutyryl cyclic AMP）和二丁酰环磷酸鸟苷（dibutyryl cyclic GMP）对ANP释放无影响。精氨酸加压素和去氧肾上腺素均可激活多磷酸肌醇系统，进而激活二酰基甘油-蛋白激酶C系统和Ca2+-Ca2+受体系统，二者均能剂量依赖性地刺激ANP释放。去氧肾上腺素刺激的ANP释放受到钙调蛋白拮抗剂N-(6-氨基己基)-5-氯-1-萘磺酰胺（W-7）和蛋白激酶C抑制剂1-(5-异喹啉磺酰基)-2-甲基哌嗪（H-7）的抑制。心房牵张刺激ANP释放，但该释放不受W-7或H-7的抑制。这些结果表明，去氧肾上腺素诱导ANP释放的机制与牵张诱导ANP释放的机制不同。
