Houchi H, Oka M, Misbahuddin M, Morita K, Nakanishi A
Biochem Pharmacol. 1987 May 1;36(9):1551-4. doi: 10.1016/0006-2952(87)90125-0.
In isolated bovine adrenal medullary cells, vasoactive intestinal polypeptide (VIP) stimulated 14C-catecholamine synthesis from 14C-tyrosine, but not from 14C-DOPA. This stimulatory effect of VIP on 14C-catecholamine synthesis was not dependent upon extracellular Ca2+. VIP did not affect the intracellular cyclic AMP (cAMP) level. The stimulatory effect of VIP on 14C-catecholamine synthesis was additive with that of carbamylcholine, which was dependent upon extracellular Ca2+, but not with that of phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA), an activator of protein kinase C. Moreover, 1-(isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, inhibited not only TPA-stimulated, but also VIP-stimulated 14C-catecholamine synthesis from 14C-tyrosine. These results suggested that VIP stimulated catecholamine synthesis by activation of tyrosine hydroxylase and that protein kinase C was involved in this stimulatory mechanism.
在分离的牛肾上腺髓质细胞中,血管活性肠肽(VIP)刺激了从¹⁴C-酪氨酸合成¹⁴C-儿茶酚胺,但不刺激从¹⁴C-多巴合成¹⁴C-儿茶酚胺。VIP对¹⁴C-儿茶酚胺合成的这种刺激作用不依赖于细胞外Ca²⁺。VIP不影响细胞内环磷酸腺苷(cAMP)水平。VIP对¹⁴C-儿茶酚胺合成的刺激作用与氨甲酰胆碱的刺激作用相加,氨甲酰胆碱的刺激作用依赖于细胞外Ca²⁺,但与佛波酯12-O-十四烷酰佛波醇13-乙酸酯(TPA)(蛋白激酶C的激活剂)的刺激作用不相加。此外,蛋白激酶C的抑制剂1-(异喹啉基磺酰基)-2-甲基哌嗪(H-7)不仅抑制TPA刺激的,也抑制VIP刺激的从¹⁴C-酪氨酸合成¹⁴C-儿茶酚胺。这些结果表明,VIP通过激活酪氨酸羟化酶刺激儿茶酚胺合成,并且蛋白激酶C参与了这种刺激机制。