| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Laboratory for Physiology and 2 Department of Anesthesiology, Vrije Universiteit University Medical Center, and 3 Department of Anesthesiology, Cardiothoracic Center, Amphia Hospital, Breda, Institute for Cardiovascular Research, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands
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 [NG-nitro-L-arginine (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.
nitric oxide electrode; endothelium; amplitude of constriction; response time
This article has been cited by other articles:
|
|
 |
|
  M. Edanaga, M. Nakayama, N. Kanaya, N. Tohse, and A. Namiki Propofol Increases Pulmonary Vascular Resistance During {alpha}-Adrenoreceptor Activation in Normal and Monocrotaline-Induced Pulmonary Hypertensive Rats Anesth. Analg., January 1, 2007; 104(1): 112 - 118. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Boer, G. P. van Nieuw Amerongen, A. B. J. Groeneveld, G. J. Scheffer, J. J. de Lange, N. Westerhof, V. W. M. van Hinsbergh, and P. Sipkema Smooth muscle F-actin disassembly and RhoA/Rho-kinase signaling during endotoxin-induced alterations in pulmonary arterial compliance Am J Physiol Lung Cell Mol Physiol, October 1, 2004; 287(4): L649 - L655. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. DiMagno, J. A. Williams, Y. Hao, S. A. Ernst, and C. Owyang Endothelial nitric oxide synthase is protective in the initiation of caerulein-induced acute pancreatitis in mice Am J Physiol Gastrointest Liver Physiol, July 1, 2004; 287(1): G80 - G87. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Bailly, A. J. Ridley, S. M. Hall, and S. G. Haworth RhoA Activation by Hypoxia in Pulmonary Arterial Smooth Muscle Cells Is Age and Site Specific Circ. Res., May 28, 2004; 94(10): 1383 - 1391. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Leblais, F. Pourageaud, M. D. Ivorra, C. Guibert, R. Marthan, and B. Muller Role of {alpha}-Adrenergic Receptors in the Effect of the {beta}-Adrenergic Receptor Ligands, CGP 12177, Bupranolol, and SR 59230A, on the Contraction of Rat Intrapulmonary Artery J. Pharmacol. Exp. Ther., April 1, 2004; 309(1): 137 - 145. [Abstract] [Full Text]
|
|
|
|
|
|
M. J. DiMagno, Y. Hao, Y. Tsunoda, J. A. Williams, and C. Owyang Secretagogue-stimulated pancreatic secretion is differentially regulated by constitutive NOS isoforms in mice Am J Physiol Gastrointest Liver Physiol, March 1, 2004; 286(3): G428 - G436. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
