岩沙海葵毒素诱导大鼠尾动脉收缩及内源性去甲肾上腺素释放

Palytoxin-induced contraction and release of endogenous noradrenaline in rat tail artery.

作者信息

Karaki H, Nagase H, Ohizumi Y, Satake N, Shibata S

机构信息

Department of Veterinary Pharmacology, Faculty of Agriculture, University of Tokyo, Bunkyo-ku.

出版信息

Br J Pharmacol. 1988 Sep;95(1):183-8. doi: 10.1111/j.1476-5381.1988.tb16563.x.

DOI:10.1111/j.1476-5381.1988.tb16563.x

PMID:2905903

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1854150/

Abstract

The mechanism of the contractile effect of a potent marine toxin, palytoxin (PTX) on the rat isolated tail artery was examined. 2. PTX (10(-7) M) induced a contraction in the tail artery which was dependent on external Ca2+. This contraction was inhibited (by 75% or more) by 10(-6) M prazosin, 2.4 x 10(-5) M bretylium and 10(-4) M 6-hydroxydopamine (6-OHDA), and partially (by 40%) by 10(-5) M indomethacin. However, this contraction was not affected by 10(-6) M tetrodotoxin (TTX), 10(-6) M nifedipine or reserpine treatment. The PTX-induced contraction in reserpine-treated artery was partially inhibited by nifedipine and indomethacin but not by prazosin. 3. Transmural electrical stimulation induced a transient contraction which was dependent on external Ca2+. The contraction induced by electrical stimulation was inhibited by TTX, prazosin, bretylium, reserpine treatment and 6-OHDA but not by nifedipine or indomethacin. 4. PTX increased the release of noradrenaline from this artery. However PTX did not release noradrenaline from reserpine-treated arteries. PTX-induced noradrenaline release was only partially inhibited by TTX or by Ca2+-free solution. 5. These results suggest that PTX has pre- and postsynaptic effects in the rat tail artery. PTX may stimulate adrenergic nerves and release noradrenaline mainly by a TTX-insensitive and Ca2+-independent mechanism and partially by a TTX-sensitive and Ca2+-dependent mechanism. Further, PTX may also release prostaglandins and depolarize smooth muscle cell membrane to induce a contraction.

摘要

研究了一种强效海洋毒素——岩沙海葵毒素（PTX）对大鼠离体尾动脉的收缩作用机制。2. PTX（10⁻⁷ M）可诱导尾动脉收缩，该收缩依赖于细胞外钙离子。10⁻⁶ M哌唑嗪、2.4×10⁻⁵ M溴苄铵和10⁻⁴ M 6-羟基多巴胺（6-OHDA）可抑制这种收缩（抑制率达75%或更高），10⁻⁵ M吲哚美辛可部分抑制（抑制率40%）。然而，这种收缩不受10⁻⁶ M河豚毒素（TTX）、10⁻⁶ M硝苯地平或利血平处理的影响。利血平处理的动脉中PTX诱导的收缩可被硝苯地平和吲哚美辛部分抑制，但不受哌唑嗪抑制。3. 跨膜电刺激可诱导短暂收缩，该收缩依赖于细胞外钙离子。电刺激诱导的收缩可被TTX、哌唑嗪、溴苄铵、利血平处理和6-OHDA抑制，但不受硝苯地平或吲哚美辛抑制。4. PTX可增加该动脉去甲肾上腺素的释放。然而，PTX不能从利血平处理的动脉中释放去甲肾上腺素。PTX诱导的去甲肾上腺素释放仅被TTX或无钙溶液部分抑制。5. 这些结果表明，PTX在大鼠尾动脉中具有突触前和突触后作用。PTX可能主要通过一种TTX不敏感且钙离子不依赖的机制刺激肾上腺素能神经并释放去甲肾上腺素，部分通过一种TTX敏感且钙离子依赖的机制。此外，PTX还可能释放前列腺素并使平滑肌细胞膜去极化以诱导收缩。