Increases in myofilament Ca2+ sensitivity resulting from stimulation of RhoA and Rho kinase represent a primary mechanism of vasoconstriction and associated pulmonary hypertension resulting from chronic hypoxia (CH). This chapter summarizes recent advances in the understanding of RhoA/Rho kinase signaling mechanisms in pulmonary vascular smooth muscle (VSM) that increase the sensitivity of the contractile apparatus to Ca2+ and contribute to vasoconstriction in this setting. Such advances include the discovery of myogenic tone in small pulmonary arteries from CH rats that contributes to vasoconstriction through a mechanism inherent to the VSM, dependent on Rho kinase-induced Ca2+ sensitization but independent of L-type voltage-gated Ca2+ channels. Additional studies have revealed an important contribution of superoxide anion (O2 -)-induced RhoA activation to both receptor-mediated and membrane depolarization-induced myofilament Ca 2+ sensitization in hypertensive pulmonary arteries. Xanthine oxidase and NADPH oxidase isoforms are potential sources of O2 - that mediate RhoA-dependent vasoconstriction and associated pulmonary hypertension. © Humana Press, a part of Springer Science+ Business Media, LLC 2010.
CITATION STYLE
Resta, T. C., Broughton, B. R. S., & Jernigan, N. L. (2010). Reactive oxygen species and RhoA signaling in vascular smooth muscle: Role in chronic hypoxia-induced pulmonary hypertension. In Advances in Experimental Medicine and Biology (Vol. 661, pp. 355–373). https://doi.org/10.1007/978-1-60761-500-2_23
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