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Articles in PresS, published online ahead of print November 8, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00093.2001
Submitted on February 9, 2001
Accepted on November 1, 2001
1 Laboratory for Physiology, VU University Medical Center, Amsterdam, Netherlands; Department of Anesthesiology, VU University Medical Center, Amsterdam, Netherlands
2 Laboratory for Physiology, VU University Medical Center, Amsterdam, Netherlands
3 Department of Anesthesiology, Cardiothoracic Center Amphia Hospital, Breda, Netherlands
4 Department of Anesthesiology, VU University Medical Center, Amsterdam, Netherlands
* To whom correspondence should be addressed. E-mail: c.boer.physiol{at}med.vu.nl.
We studied the amplitude and response time (RT; time to 50% of maximal response) of pulmonary vasoreactivity and investigated whether the characteristics of pulmonary vasoreactivity can be modulated by endothelium removal, NO synthase inhibition (NG-nitro-L-arginine; L-NA), RhoA activation (lysophosphatidic acid; LPA) and Rho kinase inhibition (Y-27632). Slow acetylcholine-induced pulmonary vasodilation (262±5 s) was not due to the RT of endothelial NO release (45-55 s) and was always longer than in renal arteries (15±4 s). The rate-determining step is located in the smooth muscle cells. This was confirmed by the existing differences between the RT of NO solution and KCl-induced renal and pulmonary vasoreactivity in endothelium-denuded arteries. We found that the pulmonary contractile amplitude increases and the RT decreases by L-NA or LPA. In contrast, Y-27632 reduced the contractile amplitude and increased the RT in pulmonary arteries. These phenomena were dependent on the contractile stimulus (phenylephrine or KCl). In conclusion, slow pulmonary vasoreactivity is a smooth muscle cell characteristic that can be enhanced by RhoA and NO or endothelium removal. These effects were counteracted by Rho kinase inhibition. We show a role for RhoA/Rho kinase and NO in the modulation of pulmonary vascular reactivity.
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