The myogenic response: established facts and attractive hypotheses

Abstract

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.

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension

“…The myogenic response has been found in a wide variety of vessels with intermediate diameter from different vascular beds, and vessel wall tension has been identified as the stimulus for the myogenic response. However, larger and very small vessels possess a relatively weak myogenic response (35). There is little published information regarding the myogenic response in pulmonary arteries.…”

Microvascular dysfunction: a direct link among BMI, waist circumference and glucose homeostasis in young overweight/obese normoglycemic women?

“…The role of endothelium in modulating the myogenic response is still controversial. 29 Considering the fact that not all the microvascular parameters studied, except TRBCV max , differed significantly among the observed groups, it is possible to propose that the balance between the production of, or response to, vasodilators/vasoconstrictors is deranged.…”

Impaired microvascular endothelial function is restored by acute lower-limb exercise in post-surgical varicose vein patients

“…This prevented us from presenting data as cutaneous vascular conductance (CVC) normalised to maximal perfusion, which Cracowski et al (Cracowski et al, 2006) believe is the optimal method of data presentation in laser Doppler studies. However, as autoregulatory processes (e.g., the myogenic response) exist to maintain a relatively constant microcirculatory flow (Schubert and Mulvany, 1999), changes in brachial artery blood pressure are unlikely to be representative of changes in microcirculatory blood pressure. We did not measure maximal perfusion because this is usually achieved through sub-dermal infusion of SNP and/or by local heating at 42-44 °C for 30 min (Cracowski et al, 2006), neither of which were appropriate to our acute exercise experimental model.…”