Role of potassium channels in relaxations of isolated canine basilar arteries to acidosis

Hiroyuki Kinoshita, Zvonimir S Katusic

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

Background and Purpose: Concentration of hydrogen ions is an important regulator of cerebral arterial tone under physiological and pathological conditions. Previous studies demonstrated that in cerebral arteries, relaxations to hypercapnia are due to decrease in extracellular pH. The present study was designed to determine the role of potassium channels in mediation of cerebral arterial relaxations induced by extracellular acidosis. Methods: Rings of canine basilar arteries without endothelium were suspended for isometric forced recording. Acidosis (pH 7.3 to 7.0) was produced by incremental addition of hydrochloric acid (1.0N). The concentration of hydrogen ions was continuously monitored with a pH meter. Results: During contractions to UTP, acidosis (pH 7.3 to 7.0) induced pH- dependent relaxations. These relaxations were abolished in arteries contracted by potassium chloride (20 mmol/L). A nonselected potassium channel inhibitor, BaCl2 (10-3 and 10-4 mol/L), and an ATP-sensitive potassium channel inhibitor, glyburide (5 x 10-6 mol/L), significantly reduced relaxations to acidosis. Furthermore, BaCl2 (10-3 mol/L) and glyburide (5 x 10-6 mol/L) abolished relaxations to an ATP-sensitive potassium channel opener, cromakalim (10-8 to 3 x 10-5 mol/L). However, these potassium channel inhibitors did not affect relaxations to a voltage- dependent calcium channel inhibitor, diltiazem (10-8 to 10-4 mol/L), and glyburide (5 x 10-6 mol/L) did not alter relaxations to a nitric oxide donor. SIN-1 (10-9 to 10-4 mol/L). A calcium-activated potassium channel inhibitor, charybdotoxin (10-7 mol/L), and a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10-3 mol/L), did not affect relaxations to acidosis. Conclusions. These results suggest that extracellular acidosis causes relaxations of cerebral arteries in part by activation of potassium channels. ATP-sensitive potassium channels appear to contribute to acidosis-induced decrease in cerebral arterial tone.

Original languageEnglish (US)
Pages (from-to)433-438
Number of pages6
JournalStroke
Volume28
Issue number2
StatePublished - Feb 1997

Fingerprint

Basilar Artery
Potassium Channels
Acidosis
Canidae
KATP Channels
Glyburide
Cerebral Arteries
Delayed Rectifier Potassium Channels
Molsidomine
Cromakalim
Charybdotoxin
Calcium-Activated Potassium Channels
4-Aminopyridine
Uridine Triphosphate
Potassium Chloride
Nitric Oxide Donors
Hypercapnia
Hydrochloric Acid
Diltiazem
Calcium Channels

Keywords

  • acidosis
  • cerebral arteries
  • dogs
  • potassium channels
  • vasodilation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

Role of potassium channels in relaxations of isolated canine basilar arteries to acidosis. / Kinoshita, Hiroyuki; Katusic, Zvonimir S.

In: Stroke, Vol. 28, No. 2, 02.1997, p. 433-438.

Research output: Contribution to journalArticle

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abstract = "Background and Purpose: Concentration of hydrogen ions is an important regulator of cerebral arterial tone under physiological and pathological conditions. Previous studies demonstrated that in cerebral arteries, relaxations to hypercapnia are due to decrease in extracellular pH. The present study was designed to determine the role of potassium channels in mediation of cerebral arterial relaxations induced by extracellular acidosis. Methods: Rings of canine basilar arteries without endothelium were suspended for isometric forced recording. Acidosis (pH 7.3 to 7.0) was produced by incremental addition of hydrochloric acid (1.0N). The concentration of hydrogen ions was continuously monitored with a pH meter. Results: During contractions to UTP, acidosis (pH 7.3 to 7.0) induced pH- dependent relaxations. These relaxations were abolished in arteries contracted by potassium chloride (20 mmol/L). A nonselected potassium channel inhibitor, BaCl2 (10-3 and 10-4 mol/L), and an ATP-sensitive potassium channel inhibitor, glyburide (5 x 10-6 mol/L), significantly reduced relaxations to acidosis. Furthermore, BaCl2 (10-3 mol/L) and glyburide (5 x 10-6 mol/L) abolished relaxations to an ATP-sensitive potassium channel opener, cromakalim (10-8 to 3 x 10-5 mol/L). However, these potassium channel inhibitors did not affect relaxations to a voltage- dependent calcium channel inhibitor, diltiazem (10-8 to 10-4 mol/L), and glyburide (5 x 10-6 mol/L) did not alter relaxations to a nitric oxide donor. SIN-1 (10-9 to 10-4 mol/L). A calcium-activated potassium channel inhibitor, charybdotoxin (10-7 mol/L), and a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10-3 mol/L), did not affect relaxations to acidosis. Conclusions. These results suggest that extracellular acidosis causes relaxations of cerebral arteries in part by activation of potassium channels. ATP-sensitive potassium channels appear to contribute to acidosis-induced decrease in cerebral arterial tone.",
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N2 - Background and Purpose: Concentration of hydrogen ions is an important regulator of cerebral arterial tone under physiological and pathological conditions. Previous studies demonstrated that in cerebral arteries, relaxations to hypercapnia are due to decrease in extracellular pH. The present study was designed to determine the role of potassium channels in mediation of cerebral arterial relaxations induced by extracellular acidosis. Methods: Rings of canine basilar arteries without endothelium were suspended for isometric forced recording. Acidosis (pH 7.3 to 7.0) was produced by incremental addition of hydrochloric acid (1.0N). The concentration of hydrogen ions was continuously monitored with a pH meter. Results: During contractions to UTP, acidosis (pH 7.3 to 7.0) induced pH- dependent relaxations. These relaxations were abolished in arteries contracted by potassium chloride (20 mmol/L). A nonselected potassium channel inhibitor, BaCl2 (10-3 and 10-4 mol/L), and an ATP-sensitive potassium channel inhibitor, glyburide (5 x 10-6 mol/L), significantly reduced relaxations to acidosis. Furthermore, BaCl2 (10-3 mol/L) and glyburide (5 x 10-6 mol/L) abolished relaxations to an ATP-sensitive potassium channel opener, cromakalim (10-8 to 3 x 10-5 mol/L). However, these potassium channel inhibitors did not affect relaxations to a voltage- dependent calcium channel inhibitor, diltiazem (10-8 to 10-4 mol/L), and glyburide (5 x 10-6 mol/L) did not alter relaxations to a nitric oxide donor. SIN-1 (10-9 to 10-4 mol/L). A calcium-activated potassium channel inhibitor, charybdotoxin (10-7 mol/L), and a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10-3 mol/L), did not affect relaxations to acidosis. Conclusions. These results suggest that extracellular acidosis causes relaxations of cerebral arteries in part by activation of potassium channels. ATP-sensitive potassium channels appear to contribute to acidosis-induced decrease in cerebral arterial tone.

AB - Background and Purpose: Concentration of hydrogen ions is an important regulator of cerebral arterial tone under physiological and pathological conditions. Previous studies demonstrated that in cerebral arteries, relaxations to hypercapnia are due to decrease in extracellular pH. The present study was designed to determine the role of potassium channels in mediation of cerebral arterial relaxations induced by extracellular acidosis. Methods: Rings of canine basilar arteries without endothelium were suspended for isometric forced recording. Acidosis (pH 7.3 to 7.0) was produced by incremental addition of hydrochloric acid (1.0N). The concentration of hydrogen ions was continuously monitored with a pH meter. Results: During contractions to UTP, acidosis (pH 7.3 to 7.0) induced pH- dependent relaxations. These relaxations were abolished in arteries contracted by potassium chloride (20 mmol/L). A nonselected potassium channel inhibitor, BaCl2 (10-3 and 10-4 mol/L), and an ATP-sensitive potassium channel inhibitor, glyburide (5 x 10-6 mol/L), significantly reduced relaxations to acidosis. Furthermore, BaCl2 (10-3 mol/L) and glyburide (5 x 10-6 mol/L) abolished relaxations to an ATP-sensitive potassium channel opener, cromakalim (10-8 to 3 x 10-5 mol/L). However, these potassium channel inhibitors did not affect relaxations to a voltage- dependent calcium channel inhibitor, diltiazem (10-8 to 10-4 mol/L), and glyburide (5 x 10-6 mol/L) did not alter relaxations to a nitric oxide donor. SIN-1 (10-9 to 10-4 mol/L). A calcium-activated potassium channel inhibitor, charybdotoxin (10-7 mol/L), and a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10-3 mol/L), did not affect relaxations to acidosis. Conclusions. These results suggest that extracellular acidosis causes relaxations of cerebral arteries in part by activation of potassium channels. ATP-sensitive potassium channels appear to contribute to acidosis-induced decrease in cerebral arterial tone.

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