Abstract
The myogenic response is an inherent property of resistance arteries that warrants a relatively constant blood flow in response to changes in perfusion pressure and protect delicate organs from vascular insufficiencies and excessive blood flow. This fundamental phenomenon has been extensively studied aiming to elucidate the underlying mechanisms triggering smooth muscle contraction in response to intraluminal pressure elevation, particularly, Rho-associated kinase (ROK)-mediated Ca2+-independent mechanisms. The size of the resistance arteries limits the capacity to examine changes in protein phosphorylation/expression levels associated with ROK signaling. A highly sensitive biochemical detection approach was beneficial in examining the role of ROK in different force generation mechanisms along the course of myogenic constriction. In this mini review, we summarize recent results showing direct evidence for the contribution of ROK in development of myogenic response at the level of mechanotransduction, myosin light chain phosphatase inhibition and dynamic actin cytoskeleton reorganization. We will also present evidence that alterations in ROK signaling could underlie the progressive loss in myogenic response in a rat model of type 2 diabetes.
Highlights
The myogenic response is an inherent property of resistance arteries that warrants a relatively constant blood flow in response to changes in perfusion pressure and protect delicate organs from vascular insufficiencies and excessive blood flow
We summarize recent results showing direct evidence for the contribution of Rho-associated kinase (ROK) in development of myogenic response at the level of mechanotransduction, myosin light chain phosphatase inhibition and dynamic actin cytoskeleton reorganization
We will present evidence that alterations in ROK signaling could underlie the progressive loss in myogenic response in a rat model of type 2 diabetes
Summary
Over 100 years ago, Bayliss (1902) elegantly demonstrated a unique property of arterioles whereby these vessels constricted in response to an increase in perfusion pressure and dilated when the internal pressure was reduced. The sum of effects of endothelial activation by blood flow, sympathetic neuronal control, and humoral factors modulates the myogenic response and sets the peripheral vascular resistance and contributes to blood pressure regulation. ROK-Mediated Mechanisms in Myogenic Constriction regulates the capillary hydrostatic pressure against fluctuations in systemic pressures stabilizing capillary flow and shielding downstream structures from the damaging effects of high intravascular pressure (Davis, 2012). Advances in the study of myogenic tone over the last two decades unfolded the crucial role of Rho-associated kinase (ROK) in the myogenic response of resistance arteries. In this mini review, we will focus on the role of ROK in myogenic constriction in health and disease condition, type 2 diabetes. We will provide a summary of our findings pertaining to the direct detection of ROK phosphorylated protein targets in the context of myogenic constriction using a highly sensitive western blotting detection technique
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