Key result
Reactive oxygen species-induced vascular contraction and Ca2+ sensitization in rat aorta are mediated through activation of the Rho/Rho kinase signaling pathway, but not Ca2+-independent PKC.
This preclinical study demonstrates that reactive oxygen species induce vascular contraction via the Rho/Rho kinase signaling pathway, providing mechanistic insight into hypertension pathogenesis.
No takes yet. Share an insight, caveat, or question.
ROS-mediated vasoconstriction via Rho kinase in rat aorta is hypothesis-generating for hypertension; leaves open translation to human therapies.
Jin et al. (2004) studied Vascular contraction / Hypertension pathogenesis. Reactive oxygen species (ROS) generated by xanthine-xanthine oxidase vs. Inhibitors (tempol, catalase, allopurinol, Y-27632, rottlerin) was evaluated on Isometric force development (vascular contraction) and MYPT1 phosphorylation. Reactive oxygen species-induced vascular contraction and Ca2+ sensitization in rat aorta are mediated through activation of the Rho/Rho kinase signaling pathway, but not Ca2+-independent PKC.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: