Faury G, Ristori M T, Verdetti J, Jacob M P, Robert L
Centre de Physiologie et Physiopathologie Cellulaires, Université Joseph-Fourier, Grenoble, France.
J Vasc Res. 1995 Mar-Apr;32(2):112-9. doi: 10.1159/000159084.
Elastin peptides are present in human blood. As elastin receptors exist on several cell types, especially endothelial cells, this investigation was carried out to study the effect of elastin peptides on vascular tone. For this purpose, rat aortic rings were mounted in an organ bath for isometric tension measurements. Elastin peptides (kappa-elastin) were added in the concentration range of 0.1 ng/ml to 1 microgram/ml, concentrations similar to those found in the circulating blood. In rat aortic rings, precontracted or not with noradrenaline (10(-6) M), elastin peptides induced an endothelium-dependent vasodilation. The pretreatment of aortic rings with N-omega-nitro-L-arginine methyl ester (10(-5) M), an inhibitor of nitric oxide (NO) production, or with indomethacin (10(-5) M), an inhibitor of cyclooxygenase, prevented elastin peptide-induced vasodilation. These findings suggest that elastin peptides act through the synthesis of prostanoids, leading to the production of NO. Moreover, this relaxant effect of elastin peptides was decreased or inhibited when aortic rings were treated with lactose (10(-5) to 10(-2) M) or laminin (10(-6) to 10(-4) mg/ml) whereas lactose or laminin was unable to inhibit acetylcholine-induced vasodilation. These findings suggest that the inhibitory effects of lactose and laminin are specific for elastin peptide receptors and are in agreement with previous studies on these receptors. As there is evidence of the degradation of elastin in several vascular diseases, the concept that elastin peptides may contribute to the control of vascular tone is discussed.
弹性蛋白肽存在于人体血液中。由于在多种细胞类型尤其是内皮细胞上存在弹性蛋白受体，因此开展了这项研究以探讨弹性蛋白肽对血管张力的影响。为此，将大鼠主动脉环安装在器官浴槽中进行等长张力测量。添加浓度范围为0.1纳克/毫升至1微克/毫升的弹性蛋白肽（κ-弹性蛋白），该浓度与循环血液中发现的浓度相似。在大鼠主动脉环中，无论是否用去甲肾上腺素（10⁻⁶摩尔/升）预收缩，弹性蛋白肽均可诱导内皮依赖性血管舒张。用一氧化氮（NO）生成抑制剂N-ω-硝基-L-精氨酸甲酯（10⁻⁵摩尔/升）或环氧合酶抑制剂吲哚美辛（10⁻⁵摩尔/升）预处理主动脉环，可阻止弹性蛋白肽诱导的血管舒张。这些发现表明，弹性蛋白肽通过前列腺素的合成发挥作用，进而导致NO的产生。此外，当用乳糖（10⁻⁵至10⁻²摩尔/升）或层粘连蛋白（10⁻⁶至10⁻⁴毫克/毫升）处理主动脉环时，弹性蛋白肽的这种舒张作用减弱或受到抑制，而乳糖或层粘连蛋白无法抑制乙酰胆碱诱导的血管舒张。这些发现表明，乳糖和层粘连蛋白的抑制作用对弹性蛋白肽受体具有特异性，并且与先前对这些受体的研究一致。鉴于有证据表明在几种血管疾病中存在弹性蛋白降解，本文讨论了弹性蛋白肽可能有助于控制血管张力的概念。
