Neuropeptide Y‐induced intracellular Ca2+ increases in vascular smooth muscle cells

FEBS Letters

Mihara, Shin-ichi¹  Shigeri, Yasushi¹  Fujimoto, Masafumi¹ 

[1] Shionogi Research Laboratories, Shionogi & Co. Ltd, 5-12-4 Sagisu Fukushima-ku, Osaka 553, Japan

关键词: Neuropeptide Y;    Cytosolic free calcium;    Pertussis toxin;    Inositol 1;    4;    5-trisphosphate;    Cyclic AMP;    (Porcine aortic smooth muscle cell);   

DOI  :  10.1016/0014-5793(89)81499-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The effect of neuropeptide Y (NPY) on cytosolic free Ca²⁺ concentration ([Ca²⁺],) was studied in cultured smooth muscle cells from porcine aorta (PASMC) and compared with the effect of bradykinin (BK) and angiotensin II (ATII) on [Ca²⁺. All peptides induced dose-dependent and transient rises in [Ca²⁺], which were not blocked by extracellular EGTA, but the NPY response was different from the others' as follows. First, the [Ca²⁺]; rise induced by NPY was not as rapid as that induced by BK or ATII. Second, pertussis toxin abolished the [Ca²⁺], rise induced by NPY, but not by BK or ATII. Third, following initial treatment with BK, PASMC were able to respond to NPY, but not to ATII. Finally, BK and ATII, but not NPY, significantly increased inositol 1,4,5-trisphosphate (Ins(l,4,5)P₃) generation. Although NPY attenuated forskolin-induced accumulation of cyclic AMP, forskolin- and 3-isobutyl-1-methyl-xanthine-induced alterations in intracellular cyclic AMP did not affect the NPY-induced [Ca²⁺]_i rise. These results suggest that'NPY increases [Ca²⁺], by a pertussis toxin-sensitive GTP binding protein-involved mechanism which is not mediated by the intracellular messengers such as Ins(1,4,5)P₃ and cyclic AMP.

【 授权许可】

Unknown