Capsaicin-Sensitive Sensory Nerves Mediate the Cellular and Microvascular Effects of H2S via TRPA1 Receptor Activation and Neuropeptide Release
Capsaicin-Sensitive Sensory Nerves Mediate the Cellular and Microvascular Effects of H2S via TRPA1 Receptor Activation and Neuropeptide Release
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DOI：
10.1007/s12031-016-0802-z
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发表时间：
2016-10-01
影响因子：
3.1
通讯作者：
Pinter, Erika
中科院分区：
文献类型：
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作者：
Hajna, Zsfia;Saghy, Eva;Pinter, Erika
据推测，TRPA 1受体可被硫化氢（H2S）激活。在此，我们研究了TRPA 1受体在H2S诱导的三叉神经节（TRG）神经元[Ca 2 +]（i）增加中的作用，以及辣椒素敏感的感觉神经在H2S诱导的皮肤血管舒张中的参与。[Ca2用比率法测定NaHS、Na 2S、异硫氰酸烯丙酯（AITC）或KCl处理后TRPA 1（+/+）和TRPA 1（-/-）小鼠TRG神经元的[+]（i）。通过激光多普勒成像检测耳内微循环变化，以响应局部NaHS、AITC、NaOH、NaSO 3或NaCl。用树脂毒素（RTX）、CGRP拮抗剂BIBN 4096、NK 1受体拮抗剂CP 99994或K+（ATP）通道阻断剂格列本脲处理小鼠。还研究了α-CGRP（-/-）和NK 1（-/-）小鼠。NaHS和Na 2S增加TRPA（+/+）小鼠TRG神经元[Ca ~（2+）]（i），但不增加TRPA 1（-/-）小鼠TRG神经元[Ca ~（2+）]（i）。NaHS增加皮肤血流量，而NaOH，NaSO 3和NaCl没有引起显着变化。在RTX处理的动物中，以及通过单独或联合使用BIBN 4096或CP 99994预处理，NaHS诱导的血管舒张减少。与野生型相比，α-CGRP（-/-）或NK 1（-/-）小鼠中NaHS诱导的血管舒张显著较小。H2S通过TRPA 1受体激活辣椒素敏感的感觉神经，并且所产生的血管舒张由血管活性感觉神经肽CGRP和P物质的释放介导。
It is supposed that TRPA1 receptor can be activated by hydrogen sulphide (H2S). Here, we have investigated the role of TRPA1 receptor in H2S-induced [Ca2+](i) increase in trigeminal ganglia (TRG) neurons, and the involvement of capsaicin-sensitive sensory nerves in H2S-evoked cutaneous vasodilatation. [Ca2+](i) was measured with ratiometric technique on TRG neurons of TRPA1(+/+) and TRPA1(-/-) mice after NaHS, Na2S, allylisothiocyanate (AITC) or KCl treatment. Microcirculatory changes in the ear were detected by laser Doppler imaging in response to topical NaHS, AITC, NaOH, NaSO3 or NaCl. Mice were either treated with resiniferatoxin (RTX), or CGRP antagonist BIBN4096, or NK1 receptor antagonist CP99994, or K+ (ATP) channel blocker glibenclamide. Alpha-CGRP(-/-) and NK1 (-/-) mice were also investigated. NaHS and Na2S increased [Ca2+](i) in TRG neurons derived from TRPA(+/+) but not from TRPA1(-/-) mice. NaHS increased cutaneous blood flow, while NaOH, NaSO3 and NaCl did not cause significant changes. NaHS-induced vasodilatation was reduced in RTX-treated animals, as well as by pre-treatment with BIBN4096 or CP99994 alone or in combination. NaHS-induced vasodilatation was significantly smaller in alpha-CGRP(-/-) or NK1 (-/-) mice compared to wild-types. H2S activates capsaicin-sensitive sensory nerves through TRPA1 receptors and the resultant vasodilatation is mediated by the release of vasoactive sensory neuropeptides CGRP and substance P.