Schubert R, Mulvany M J
Institute of Physiology, University of Rostock, PSF 100888, D-18055 Rostock, Germany.
Clin Sci (Lond). 1999 Apr;96(4):313-26.
The myogenic response of small arteries and arterioles has been shown to contribute significantly to autoregulation in different vascular beds. It is characterized by a constriction of the vessel after an increase of transmural pressure and a dilation of the vessel after a decrease of transmural pressure. This review examines the evidence for the mechanisms of the myogenic response, with the aim of distinguishing between facts and hypotheses. It appears to be established that the myogenic response is stimulated by an alteration of vessel wall tension, that it does not require the presence of the endothelium and, for pressure increases, that it is accompanied by a membrane depolarization and an increase of the intracellular Ca2+ concentration, which depends largely on an influx of extracellular calcium via voltage-operated calcium channels. Under in vitro conditions, it may further be considered an established fact that the myogenic response can be modulated by transmitters, like noradrenaline, and factors released from the endothelium upon its activation. In contrast, many other aspects of the myogenic response remain hypothetical. Thus, the mechanism of the depolarization, its importance for the development of the myogenic response, the participation of other pathways for calcium influx, and the role of an intracellular calcium release in the myogenic response are still under debate. Furthermore, the participation of a variety of intracellular second messenger systems in the myogenic response, i.e. inositol trisphosphate, diacylglycerol, phospholipase A2, protein kinase C or 20-hydroxyeicosatetraenoic acid, is still unclear. Additionally, the roles of the pulsatility of the blood pressure and of remote signals from neighbouring vessel segments as well as of different metabolites are not clarified. This review suggests that while the primary mechanisms of the myogenic response are well understood, the details of the signalling pathways are still undefined. The clinical significance of the myogenic response remains to be determined.
小动脉和微动脉的肌源性反应已被证明对不同血管床的自身调节有重要作用。其特征是跨壁压升高后血管收缩,跨壁压降低后血管扩张。本综述研究了肌源性反应机制的证据,目的是区分事实与假设。似乎已经确定,肌源性反应是由血管壁张力的改变所刺激,它不需要内皮细胞的存在,并且对于压力升高而言,它伴随着膜去极化和细胞内Ca2+浓度的增加,这在很大程度上取决于通过电压门控钙通道的细胞外钙内流。在体外条件下,还可以认为肌源性反应可被递质(如去甲肾上腺素)以及内皮细胞激活后释放的因子所调节这一事实是成立的。相比之下,肌源性反应的许多其他方面仍然是假设性的。因此,去极化的机制、其对肌源性反应发展的重要性、其他钙内流途径的参与以及细胞内钙释放在肌源性反应中的作用仍在争论中。此外,多种细胞内第二信使系统(即肌醇三磷酸、二酰甘油、磷脂酶A2、蛋白激酶C或20-羟基二十碳四烯酸)在肌源性反应中的参与情况仍不清楚。另外,血压的脉动性、来自相邻血管段的远程信号以及不同代谢产物的作用也未阐明。本综述表明,虽然肌源性反应的主要机制已得到很好的理解,但信号通路的细节仍不明确。肌源性反应的临床意义仍有待确定。