Karimian M, Ferrell W R
Institute of Physiology, University of Glasgow, UK.
Neurosci Lett. 1994 Jan 17;166(1):39-42. doi: 10.1016/0304-3940(94)90835-4.
In previous experiments, intra-articular administration of calcitonin gene-related peptide (CGRP) failed to elicit plasma protein extravasation into synovial fluid. In the present study, using a sensitive technique to assay protein in synovial fluid, intra-articular perfusion of CGRP (10(-6) M) was found to produce protein extravasation which was sustained throughout the period of infusion. Both lower (10(-7) M) and higher (10(-5) M) concentrations of CGRP failed to produce extravasation. This failure at the highest concentration of CGRP was the likely consequence of a significant fall in arterial blood pressure which occurred with administration of CGRP at this concentration. In the presence of arterial hypotension induced by an alpha-adrenoceptor antagonist, 10(-6) M CGRP failed to produce extravasation. Plasma extravasation induced by CGRP was a specific effect and not merely a consequence of its potent vasodilator properties as similar vasodilator responses induced by a beta-adrenoceptor agonist failed to induce protein leakage. These findings indicate that CGRP can alter blood vessel permeability and therefore could additionally contribute to neurally mediated inflammatory responses.
在先前的实验中，关节内注射降钙素基因相关肽（CGRP）未能引起血浆蛋白渗入滑液。在本研究中，使用一种灵敏的技术检测滑液中的蛋白质，发现关节内灌注CGRP（10⁻⁶ M）会产生蛋白外渗，且在整个输注期间持续存在。较低浓度（10⁻⁷ M）和较高浓度（10⁻⁵ M）的CGRP均未能产生外渗。CGRP最高浓度时未能产生外渗，可能是由于在此浓度下注射CGRP会导致动脉血压显著下降。在α肾上腺素能受体拮抗剂诱导的动脉低血压情况下，10⁻⁶ M的CGRP未能产生外渗。CGRP诱导的血浆外渗是一种特异性效应，并非仅仅是其强大的血管舒张特性的结果，因为β肾上腺素能受体激动剂诱导的类似血管舒张反应未能诱导蛋白渗漏。这些发现表明，CGRP可以改变血管通透性，因此可能额外促成神经介导的炎症反应。
