In the last few decades, a substantial body of evidence underlined the pivotal role of bradykinin in certain types of angioedema. The formation and breakdown of bradykinin has been studied thoroughly; however, numerous questions remained open regarding the triggering, course, and termination of angioedema attacks. Recently, it became clear that vascular endothelial cells have an integrative role in the regulation of vessel permeability. Apart from bradykinin, a great number of factors of different origin, structure, and mechanism of action are capable of modifying the integrity of vascular endothelium, and thus, may participate in the regulation of angioedema formation. Our aim in this review is to describe the most important permeability factors and the molecular mechanisms how they act on endothelial cells. Based on endothelial cell function, we also attempt to explain some of the challenging findings regarding bradykinin-mediated angioedema, where the function of bradykinin itself cannot account for the pathophysiology. By deciphering the complex scenario of vascular permeability regulation and edema formation, we may gain better scientific tools to be able to predict and treat not only bradykinin-mediated but other types of angioedema as well.

在过去的几十年里，大量证据强调了缓激肽在某些类型的血管性水肿中的关键作用。缓激肽的形成和分解已经过深入研究；然而，许多关于血管性水肿发作的触发、过程和终止的问题仍然悬而未决。最近，很明显血管内皮细胞在血管通透性的调节中具有综合作用。除缓激肽外，许多不同来源、结构和作用机制的因子都能够改变血管内皮的完整性，因此可能参与血管性水肿形成的调节。我们在这篇综述中的目的是描述最重要的渗透性因素以及它们如何作用于内皮细胞的分子机制。基于内皮细胞功能，我们还试图解释有关缓激肽介导的血管性水肿的一些具有挑战性的发现，其中缓激肽本身的功能无法解释病理生理学。通过破译血管通透性调节和水肿形成的复杂情况，我们可以获得更好的科学工具，不仅能够预测和治疗缓激肽介导的血管性水肿，还能够预测和治疗其他类型的血管性水肿。