Cystic fibrosis, vasoactive intestinal polypeptide, and active cutaneous vasodilation.
Cystic fibrosis, vasoactive intestinal polypeptide, and active cutaneous vasodilation.
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囊性纤维化、血管活性肠多肽和活性皮肤血管舒张。
DOI：
10.1152/jappl.1990.69.6.2149
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Freund,PR
中科院分区：
文献类型：
--
作者：
Savage,MV;Brengelmann,GL;Buchan,AM;Freund,PR
人类体温过高时伴随出汗的主动皮肤血管扩张的传递物质尚不清楚。284：515-521,180)假设是血管活性肠肽(VIP)与乙酰胆碱共传递。DC 229：1407-1408,1985)报道囊性纤维化症患者皮肤中VIP神经分布稀疏。在这些受试者中，主动血管扩张的相应减弱将是VIP参与人体体温调节的效应机制的证据。4例CF患者皮肤活检的免疫细胞化学分析证实VIP神经支配稀疏。我们还分析了降钙素基因相关肽(CGRP；正常)、P物质(正常)和神经肽Y(低)的免疫反应性。尽管VIP免疫反应神经分布稀少，但我们的CF受试者的皮肤血管对高温的反应是正常的。由于VIP并非完全缺失，这一证据不足以排除VIP是血管扩张剂递质的可能性。然而，我们观察到的CGRP和P物质的神经支配可能意味着这两种多肽中的一种或两种的释放是充分发展的主动皮肤血管扩张的机制。
The transmitter substance for the active cutaneous vasodilation that accompanies sweating during hyperthermia in humans is unknown. Hokfelt et al. (Nature Lond. 284: 515-521, 180) hypothesized that it is vasoactive intestinal polypeptide (VIP) that is cotransmitted with acetylcholine. Heinz-Erian et al. (Science Wash. DC 229: 1407-1408, 1985) reported that VIP innervation is sparse in the skin of persons with cystic fibrosis (CF). A corresponding attenuation of active vasodilation in these subjects would be evidence that VIP is involved in this effector mechanism of human thermor-regulation. Immunocytochemical analysis of skin biopsies from four men with CF confirmed that VIP innervation was sparse. We also analyzed immunoreactivity for calcitonin gene-related peptide (CGRP; normal), substance P (normal), and neuropeptide Y (low). VIP-immunoreactive Merkel cells were abnormal. Despite sparse VIP-immunoreactive innervation, our CF subjects' cutaneous vascular responses to hyperthermia were normal. Because VIP was not completely absent, this evidence is insufficient to rule out VIP as the vasodilator transmitter. However, the CGRP and substance P innervation we observed could mean that release of one or both of these peptides was the mechanism of the fully developed active cutaneous vasodilation.