Is actin depolymerization the mechanism that causes vasodilation in small resistance arterioles? Listen as Associate Editor Robert Hester (University of Mississippi Medical Center) and content expert William Jackson (Michigan State University) interview lead author Philip Clifford (University of Illinois at Chicago) about the new study by Clifford et al. Using two different vasodilators with two different mechanisms of action, Clifford and co-authors found that there was an increase in the G-actin to sm22apha ratio, signaling a reduction in the amount of F-actin in the cell. Both vasodilators investigated-- pinacidil and sodium nitroprusside—act partially through an actin depolymerization. However, sodium nitroprusside is more dependent on this mechanism to achieve vasodilation. What is the time course of this change in actin polymerization? Is depolymerization essential for vasodilation, or a by-product of vasodilation? Listen to our experts and find out.
Philip S. Clifford, Brian S. Ferguson, Jeffrey L. Jasperse, and Michael A. Hill Arteriolar vasodilation involves actin depolymerization Am J Physiol Heart Circ Physiol, published August 8, 2018. DOI: 10.1152/ajpheart.00723.2017