Potassium channels modulate canine pulmonary vasoreactivity to protein kinase C activation

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

The role of Ca 2+ -activated K + -channel, ATP-sensitive K + -channel, and delayed rectifier K + -channel modulation in the canine pulmonary vascular response to protein kinase C (PKC) activation was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. The PKC activators phorbol 12-myristate 13-acetate (PMA; 10 -7 M) and thymeleatoxin (THX; 10 -7 M) significantly increased pulmonary arterial and pulmonary venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. The Ca 2+ -activated K + -channel blocker tetraethylammonium ions (1 mM), the ATP-sensitive K + -channel inhibitor glibenclamide (10 -5 M), and the delayed rectifier K + -channel blocker 4-aminopyridine (10 -4 M) potentiated the pressor response to both PMA and THX on the arterial and venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K + -channel opener cromakalim (10 -5 M) attenuated the vasoconstrictor effect of PMA and THX on both the arterial and venous vessels. In addition, membrane depolarization by 30 mM KCl elicited an increase in the pressor response to PMA. These results indicate that pharmacological activation of PKC elicits pulmonary vasoconstriction. Closure of the Ca 2+ -activated K + channels, ATP-sensitive K + channels, and delayed rectifier K + channels as well as direct membrane depolarization by KCl potentiated the response to PMA and THX, indicating that K + channels modulate the canine pulmonary vasoconstrictor response to PKC activation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume277
Issue number3 PART 1
StatePublished - Sep 1 1999

Fingerprint

Potassium Channels
Protein Kinase C
Canidae
Lung
Blood Vessels
Adenosine Triphosphate
Compliance
Vasoconstrictor Agents
Capillary Resistance
Cromakalim
Lung Compliance
4-Aminopyridine
Tetraethylammonium
Membranes
Glyburide
Vasoconstriction
Vascular Resistance
Acetates
Pharmacology
Dogs

Keywords

  • Pulmonary vascular compliance
  • Pulmonary vascular resistance
  • Thymeleatoxin

ASJC Scopus subject areas

  • Physiology (medical)

Cite this

Potassium channels modulate canine pulmonary vasoreactivity to protein kinase C activation. / Barman, Scott A.

In: American Journal of Physiology, Vol. 277, No. 3 PART 1, 01.09.1999.

Research output: Contribution to journalArticle

@article{923353321da1434db63d69af963edfe8,
title = "Potassium channels modulate canine pulmonary vasoreactivity to protein kinase C activation",
abstract = "The role of Ca 2+ -activated K + -channel, ATP-sensitive K + -channel, and delayed rectifier K + -channel modulation in the canine pulmonary vascular response to protein kinase C (PKC) activation was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. The PKC activators phorbol 12-myristate 13-acetate (PMA; 10 -7 M) and thymeleatoxin (THX; 10 -7 M) significantly increased pulmonary arterial and pulmonary venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. The Ca 2+ -activated K + -channel blocker tetraethylammonium ions (1 mM), the ATP-sensitive K + -channel inhibitor glibenclamide (10 -5 M), and the delayed rectifier K + -channel blocker 4-aminopyridine (10 -4 M) potentiated the pressor response to both PMA and THX on the arterial and venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K + -channel opener cromakalim (10 -5 M) attenuated the vasoconstrictor effect of PMA and THX on both the arterial and venous vessels. In addition, membrane depolarization by 30 mM KCl elicited an increase in the pressor response to PMA. These results indicate that pharmacological activation of PKC elicits pulmonary vasoconstriction. Closure of the Ca 2+ -activated K + channels, ATP-sensitive K + channels, and delayed rectifier K + channels as well as direct membrane depolarization by KCl potentiated the response to PMA and THX, indicating that K + channels modulate the canine pulmonary vasoconstrictor response to PKC activation.",
keywords = "Pulmonary vascular compliance, Pulmonary vascular resistance, Thymeleatoxin",
author = "Barman, {Scott A}",
year = "1999",
month = "9",
day = "1",
language = "English (US)",
volume = "277",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3 PART 1",

}

TY - JOUR

T1 - Potassium channels modulate canine pulmonary vasoreactivity to protein kinase C activation

AU - Barman, Scott A

PY - 1999/9/1

Y1 - 1999/9/1

N2 - The role of Ca 2+ -activated K + -channel, ATP-sensitive K + -channel, and delayed rectifier K + -channel modulation in the canine pulmonary vascular response to protein kinase C (PKC) activation was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. The PKC activators phorbol 12-myristate 13-acetate (PMA; 10 -7 M) and thymeleatoxin (THX; 10 -7 M) significantly increased pulmonary arterial and pulmonary venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. The Ca 2+ -activated K + -channel blocker tetraethylammonium ions (1 mM), the ATP-sensitive K + -channel inhibitor glibenclamide (10 -5 M), and the delayed rectifier K + -channel blocker 4-aminopyridine (10 -4 M) potentiated the pressor response to both PMA and THX on the arterial and venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K + -channel opener cromakalim (10 -5 M) attenuated the vasoconstrictor effect of PMA and THX on both the arterial and venous vessels. In addition, membrane depolarization by 30 mM KCl elicited an increase in the pressor response to PMA. These results indicate that pharmacological activation of PKC elicits pulmonary vasoconstriction. Closure of the Ca 2+ -activated K + channels, ATP-sensitive K + channels, and delayed rectifier K + channels as well as direct membrane depolarization by KCl potentiated the response to PMA and THX, indicating that K + channels modulate the canine pulmonary vasoconstrictor response to PKC activation.

AB - The role of Ca 2+ -activated K + -channel, ATP-sensitive K + -channel, and delayed rectifier K + -channel modulation in the canine pulmonary vascular response to protein kinase C (PKC) activation was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. The PKC activators phorbol 12-myristate 13-acetate (PMA; 10 -7 M) and thymeleatoxin (THX; 10 -7 M) significantly increased pulmonary arterial and pulmonary venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. The Ca 2+ -activated K + -channel blocker tetraethylammonium ions (1 mM), the ATP-sensitive K + -channel inhibitor glibenclamide (10 -5 M), and the delayed rectifier K + -channel blocker 4-aminopyridine (10 -4 M) potentiated the pressor response to both PMA and THX on the arterial and venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K + -channel opener cromakalim (10 -5 M) attenuated the vasoconstrictor effect of PMA and THX on both the arterial and venous vessels. In addition, membrane depolarization by 30 mM KCl elicited an increase in the pressor response to PMA. These results indicate that pharmacological activation of PKC elicits pulmonary vasoconstriction. Closure of the Ca 2+ -activated K + channels, ATP-sensitive K + channels, and delayed rectifier K + channels as well as direct membrane depolarization by KCl potentiated the response to PMA and THX, indicating that K + channels modulate the canine pulmonary vasoconstrictor response to PKC activation.

KW - Pulmonary vascular compliance

KW - Pulmonary vascular resistance

KW - Thymeleatoxin

UR - http://www.scopus.com/inward/record.url?scp=0032888677&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032888677&partnerID=8YFLogxK

M3 - Article

VL - 277

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 3 PART 1

ER -