AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 275: L64-L70, 1998;
1040-0605/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barman, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barman, S. A.
Vol. 275, Issue 1, L64-L70, July 1998

Potassium channels modulate hypoxic pulmonary vasoconstriction

Scott A. Barman

Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912

The role of Ca2+-activated K+-channel, ATP-sensitive K+-channel, and delayed rectifier K+-channel modulation in the canine pulmonary vascular response to hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. Under normoxia, the Ca2+-activated K+-channel blocker tetraethylammonium (1 mM), the ATP-sensitive K+-channel inhibitor glibenclamide (10-5 M), and the delayed rectifier K+-channel blocker 4-aminopyridine (10-4 M) elicited a small but significant increase in pulmonary arterial pressure. Hypoxia significantly increased pulmonary arterial and venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. Tetraethylammonium, glibenclamide, and 4-aminopyridine potentiated the response to hypoxia on the arterial segments but not on the venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K+-channel opener cromakalim and the L-type voltage-dependent Ca2+-channel blocker verapamil (10-5 M) inhibited the vasoconstrictor effect of hypoxia on both the arterial and venous vessels. These results indicate that closure of the Ca2+-activated K+ channels, ATP-sensitive K+ channels, and delayed rectifier K+ channels potentiate the canine pulmonary arterial response under hypoxic conditions and that L-type voltage-dependent Ca2+ channels modulate hypoxic vasoconstriction. Therefore, the possibility exists that K+-channel inhibition is a key event that links hypoxia to pulmonary vasoconstriction by eliciting membrane depolarization and subsequent Ca2+-channel activation, leading to Ca2+ influx.

hypoxia; pulmonary vascular resistance; pulmonary vascular compliance; verapamil; tetraethylammonium; cromakalim; glibenclamide


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Wang, L. A. Shimoda, L. Weigand, W. Wang, D. Sun, and J. T. Sylvester
Acute hypoxia increases intracellular [Ca2+] in pulmonary arterial smooth muscle by enhancing capacitative Ca2+ entry
Am J Physiol Lung Cell Mol Physiol, June 1, 2005; 288(6): L1059 - L1069.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
B. M. Tsai, M. Wang, J. M. Pitcher, K. K. Meldrum, and D. R. Meldrum
Hypoxic pulmonary vasoconstriction and pulmonary artery tissue cytokine expression are mediated by protein kinase C
Am J Physiol Lung Cell Mol Physiol, December 1, 2004; 287(6): L1215 - L1219.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
C. Hohne, M. O. Krebs, M. Seiferheld, W. Boemke, G. Kaczmarczyk, and E. R. Swenson
Acetazolamide prevents hypoxic pulmonary vasoconstriction in conscious dogs
J Appl Physiol, August 1, 2004; 97(2): 515 - 521.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
Y. Morio and I. F. McMurtry
Ca2+ release from ryanodine-sensitive store contributes to mechanism of hypoxic vasoconstriction in rat lungs
J Appl Physiol, February 1, 2002; 92(2): 527 - 534.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. S. Naik and B. R. Walker
Homogeneous segmental profile of carbon monoxide-mediated pulmonary vasodilation in rats
Am J Physiol Lung Cell Mol Physiol, December 1, 2001; 281(6): L1436 - L1443.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. A. Coppock, J. R. Martens, and M. M. Tamkun
Molecular basis of hypoxia-induced pulmonary vasoconstriction: role of voltage-gated K+ channels
Am J Physiol Lung Cell Mol Physiol, July 1, 2001; 281(1): L1 - L12.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. P. Carter, K. Sato, Y. Morio, and I. F. McMurtry
Inhibition of KCa channels restores blunted hypoxic pulmonary vasoconstriction in rats with cirrhosis
Am J Physiol Lung Cell Mol Physiol, November 1, 2000; 279(5): L903 - L910.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
K. Sato, Y. Morio, K. G. Morris, D. M. Rodman, and I. F. McMurtry
Mechanism of hypoxic pulmonary vasoconstriction involves ETA receptor-mediated inhibition of KATP channel
Am J Physiol Lung Cell Mol Physiol, March 1, 2000; 278(3): L434 - L442.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
G. B. Waypa, N. S. Chandel, and P. T. Schumacker
Model for Hypoxic Pulmonary Vasoconstriction Involving Mitochondrial Oxygen Sensing
Circ. Res., June 22, 2001; 88(12): 1259 - 1266.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online