RhoA/Rho kinase and nitric oxide modulate the agonist-induced pulmonary artery diameter response time

Christa Boer, Peter J.W. Van Der Linden, Gert Jan Scheffer, Nico Westerhof, Jaap J. De Lange, Pieter Sipkema

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18 Citations (Scopus)


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 could be modulated by endothelium removal, nitric oxide (NO) synthase inhibition [N G-nitro-Larginine (L-NNA)], 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 RT 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 the 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-NNA 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.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number3 51-3
Publication statusPublished - 29 Jun 2002


  • Amplitude of constriction
  • Endothelium
  • Nitric oxide electrode
  • Response time

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