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Am J Physiol Lung Cell Mol Physiol (September 26, 2003). doi:10.1152/ajplung.00219.2003
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Submitted on July 7, 2003
Accepted on September 23, 2003

Smooth muscle F-actin disassembly and RhoA/Rho kinase signaling during endotoxin-induced alterations in pulmonary arterial compliance

Christa Boer1*, Geerten P. van Nieuw Amerongen2, AB Johan Groeneveld3, Gert Jan Scheffer4, Jaap J. de Lange5, Nico Westerhof2, Victor WM. van Hinsbergh6, and Pieter Sipkema2

1 Laboratory for Physiology, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands; Department of Anesthesiology, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands
2 Laboratory for Physiology, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands
3 Department of Intensive Care, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands
4 Department of Anesthesiology, UMC St. Radboud, Nijmegen, The Netherlands
5 Department of Anesthesiology, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands
6 Laboratory for Physiology, VU University Medical Center, Institute for Cardiovascular Research Vrije Universiteit, Amsterdam, The Netherlands; Gaubius Laboratory TNO-PG, Leiden, The Netherlands

* To whom correspondence should be addressed. E-mail: boer{at}physiol.med.vu.nl.

Endotoxemia is associated with changed pulmonary vascular function with respect to vasoreactivity, endothelial permeability and activation of inducible nitric oxide synthase II (NOSII). However, whether altered passive arterial wall mechanics contribute to this endotoxic-induced pulmonary vascular dysfunction is still unknown. Therefore, we investigated whether endotoxin affects the passive arterial mechanics and compliance of isolated rat pulmonary arteries. Pulmonary arteries of pentobarbital anesthetized Wistar rats (n = 55) were isolated and exposed to Escherichia coli endotoxin (50 µg x ml-1) for 20 hours. Endotoxin increased pulmonary artery diameter and compliance (transmural pressure = 13 mm Hg) in an endothelium, Ca2+ or NOSII-induced NO release-independent manner. Interestingly, the endotoxin-induced alterations in the passive arterial mechanics were accompanied by disassembly of the smooth muscle cell (SMC) F-actin cytoskeleton. Disassembly of F-actin by incubation of control arteries with the cytoskeleton disrupting agent cytochalasin B or the Rho kinase inhibitor Y-27632 induced a similar increase in passive arterial diameter and compliance. In contrast, RhoA activation by lysophosphatidic acid (LPA) prevented the endotoxin-induced alterations in the pulmonary SMC F-actin cytoskeleton and passive mechanics. In conclusion, these findings indicate that disassembly of the SMC F-actin cytoskeleton and RhoA/Rho kinase signaling act as mediators of endotoxin-induced changes in the pulmonary arterial mechanics. They imply the involvement of F-actin rearrangement and RhoA/Rho kinase signaling in endotoxemia-induced vascular lung injury.




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