Pressure and flow‐dependent vascular tone

Abstract

Most small arteries are partially constricted in vivo. After excluding neurogenic, metabolic, and circulating as well as local hormonal influences, a sizeable component of tone persists which is commonly called basal tone. In the absence of such tone, cardiac output would be insufficient to maintain the circulation. This review focuses on the contribution of stretch, induced by changes in transmural pressure, and flow acting through shear forces exerted at the blood vessel wall interface, to basal tone. Evidence concerning the cellular processes that may be activated by these physical forces--the mechanotransducing systems--are discussed. The involvement of the endothelium and the role of change in membrane potential are evaluated and lead to the conclusion that pressure and flow effects do not depend exclusively on the release of endothelial factors nor the activation of voltage-gated Ca2+ channels. Stretch/pressure-induced changes in tone show distinctive pharmacological profiles. They are dependent on extracellular calcium and yet in many instances are only weakly affected by organic Ca(2+)-entry inhibitors. Flow-dependent vascular effects, both constrictor and dilator, are both exquisitely sensitive to changes in extracellular Na+ and appear to be related to its transmembrane gradient. Stretch/pressure cause activation of protein kinase C, an intracellular modulator of Ca(2+)-dependent contractile processes. The existence of separate and distinctive cellular sensing and responding systems to pressure and flow raise the possibility that the smooth muscle tone of the vascular system can be influenced independently by the pressure and rate of flow of the blood.

Activation of AT 2 Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries

“…Key Words: blood vessels Ⅲ myogenic Ⅲ arteries Ⅲ stress, mechanical Ⅲ angiotensin II Ⅲ bradykinin F low (shear stress)-induced vasodilation and pressure (tensile stress)-induced tone (myogenic tone) play a key role in the control of vascular tone. [1][2][3][4][5][6] In resistance arteries, pressure or stretch induces myogenic tone, 6 -8 which is opposed by flow-induced dilation, in vitro as well as in vivo. 3,5,6,8,9 Whereas myogenic tone is mainly independent of endothelial factors, 6,8 shear stress has been widely shown to induce the release of endothelium-derived vasoactive agents.…”

“…[1][2][3][4][5][6] In resistance arteries, pressure or stretch induces myogenic tone, 6 -8 which is opposed by flow-induced dilation, in vitro as well as in vivo. 3,5,6,8,9 Whereas myogenic tone is mainly independent of endothelial factors, 6,8 shear stress has been widely shown to induce the release of endothelium-derived vasoactive agents. 1,4,5,10,11 The local tissue renin-angiotensin system [12][13][14] is another potent regulator of vascular tone.…”

Reactivity of the isolated perfused rat tail vascular bed

“…Flow has been described as a stimulus for the endothelial cells to liberate vasodilator substances (9-11). On the other hand, the increase in pressure stretches the endothelial layer, inducing the release of endotheliumderived contraction factor (EDCF) (9,10,12). In our protocol, the increase in pressure may release endothelial EDCF that acts synergistically with PE by potentiating the pressure increment produced by flow.…”

Effects of Shear Stress on [Ca2+]I and Membrane Potential of Vascular Endothelium of Intact Rat Blood Vessels

“…The involvement of intralumenal flow in the regulation of vascular tone has long been recognised (for reviews, see Bevan & Laher, 1991;Davies, 1995). Shear stress is responsible for a significant proportion of the NO production in the vascular system (Miller & Vanhoutte, 1988).…”