| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Symposium Reports |
1 Department of Asthma, Allergy and Respiratory Science, GKT Medical and Dental School, King's College London, London SE1 1UL, UK
The pulmonary circulation differs from the systemic in several important aspects, the most important being that pulmonary arteries constrict to moderate physiological (
20–60 mmHg PO2) hypoxia, whereas systemic arteries vasodilate. This phenomenon is called hypoxic pulmonary vasoconstriction (HPV), and is responsible for maintaining the ventilation–perfusion ratio during localized alveolar hypoxia. In disease, however, global hypoxia results in a detrimental increase in total pulmonary vascular resistance, and increased load on the right heart. Despite many years of study, the precise mechanisms underlying HPV remain unresolved. However, as we argue below, there is now overwhelming evidence that hypoxia can stimulate several pathways leading to a rise in the intracellular Ca2+ concentration ([Ca2+]i) in pulmonary artery smooth muscle cells (PASMC). This rise in [Ca2+]i is consistently found to be relatively small, and HPV seems also to require rho kinase-mediated Ca2+ sensitization. There is good evidence that HPV also has an as yet unexplained endothelium dependency. In this brief review, we highlight selected recent findings and ongoing controversies which continue to animate the study of this remarkable and unique response of the pulmonary vasculature to hypoxia.
(Received 16 September 2005;
accepted after revision 21 October 2005;
first published online 27 October 2005)
Corresponding author P. Aaronson: Department of Asthma, Allergy and Respiratory Science, New Hunt's House, Guy's Hospital Campus, King's College London, London SE1 1UL, UK. Email: philip.aaronson{at}kcl.ac.uk
This article has been cited by other articles:
|
|
 |
|
  A. L. Firth, K. H. Yuill, and S. V. Smirnov Mitochondria-dependent regulation of Kv currents in rat pulmonary artery smooth muscle cells Am J Physiol Lung Cell Mol Physiol, July 1, 2008; 295(1): L61 - L70. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. L. Whitfield, E. L. Kreimier, F. C. Verdial, N. Skovgaard, and K. R. Olson Reappraisal of H2S/sulfide concentration in vertebrate blood and its potential significance in ischemic preconditioning and vascular signaling Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2008; 294(6): R1930 - R1937. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Weissmann Hypoxia-driven mechanisms in lung biology and disease: a new review series of the ERS Lung Science Conference Eur. Respir. J., April 1, 2008; 31(4): 697 - 698. [Full Text] [PDF]
|
|
|
|
|
|
R. Liu, Y. Hotta, A. R. Graveline, O. V. Evgenov, E. S. Buys, K. D. Bloch, F. Ichinose, and W. M. Zapol Congenital NOS2 deficiency prevents impairment of hypoxic pulmonary vasoconstriction in murine ventilator-induced lung injury Am J Physiol Lung Cell Mol Physiol, November 1, 2007; 293(5): L1300 - L1305. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Platoshyn, Y. Yu, E. A Ko, C. V. Remillard, and J. X.-J. Yuan Heterogeneity of hypoxia-mediated decrease in IK(V) and increase in [Ca2+]cyt in pulmonary artery smooth muscle cells Am J Physiol Lung Cell Mol Physiol, August 1, 2007; 293(2): L402 - L416. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Zhao, A. Adebiyi, Q. Xi, and J. H. Jaggar Hypoxia reduces KCa channel activity by inducing Ca2+ spark uncoupling in cerebral artery smooth muscle cells Am J Physiol Cell Physiol, June 1, 2007; 292(6): C2122 - C2128. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Y. Rochefort and E. D. Michelakis COUNTERPOINT: RELEASE OF AN ENDOTHELIUM-DERIVED VASOCONSTRICTOR AND RHOA/RHO KINASE-MEDIATED CALCIUM SENSITIZATION OF SMOOTH MUSCLE CELL CONTRACTION ARE NOT THE MAIN EFFECTORS FOR FULL AND SUSTAINED HPV J Appl Physiol, May 1, 2007; 102(5): 2072 - 2075. [Full Text] [PDF]
|
|
|
|
|
|
T. P. Robertson Point: Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction J Appl Physiol, May 1, 2007; 102(5): 2071 - 2072. [Full Text] [PDF]
|
|
|
|
|
|
C. Hohne, P. A. Pickerodt, R. C. Francis, W. Boemke, and E. R. Swenson Pulmonary vasodilation by acetazolamide during hypoxia is unrelated to carbonic anhydrase inhibition Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L178 - L184. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. K. Weir and S. L. Archer COUNTERPOINT: HYPOXIC PULMONARY VASOCONSTRICTION IS NOT MEDIATED BY INCREASED PRODUCTION OF REACTIVE OXYGEN SPECIES J Appl Physiol, September 1, 2006; 101(3): 995 - 998. [Full Text] [PDF]
|
|
|
|
|
|
Rebuttal from dr. Ward. J Appl Physiol, September 1, 2006; 101(3): 998 - 998. [Full Text] [PDF]
|
|
|
|
 |
|
 N. Weissmann, N. Sommer, R. T. Schermuly, H. A. Ghofrani, W. Seeger, and F. Grimminger Oxygen sensors in hypoxic pulmonary vasoconstriction Cardiovasc Res, September 1, 2006; 71(4): 620 - 629. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. I. Aaronson TRPC Channel Upregulation in Chronically Hypoxic Pulmonary Arteries: The HIF-1 Bandwagon Gathers Steam Circ. Res., June 23, 2006; 98(12): 1465 - 1467. [Full Text] [PDF]
|
|
|
|
 |
|
 V. A. Snetkov, G. A Knock, L. Baxter, G. D. Thomas, J. P. T. Ward, and P. I. Aaronson Mechanisms of the prostaglandin F2{alpha}-induced rise in [Ca2+]i in rat intrapulmonary arteries J. Physiol., February 15, 2006; 571(1): 147 - 163. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Beech Ions in smooth muscle, now and then J. Physiol., January 1, 2006; 570(1): 3 - 3. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
