Ca2+-activated Cl- and K+ channels and their modulation by endothelin-1 in rat pulmonary arterial smooth muscle cells

K. J. Salter, J. L. Turner, S. Albarwani, L. H. Clapp, R. Z. Kozlowski

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Using the patch-clamp recording technique, we observed that endothelin-1 (ET-1; 0.8-16 nM) enhanced a voltage-activated outward current (I(out)) and induced periodic oscillations of inward current in smooth muscle cells isolated from small pulmonary arteries (200-400 μm in diameter). Anion substitution experiments revealed that the ET-1-induced inward current was carried by Cl- ions. Application of bosentan (10 μM; an ET(A) and ET(B) receptor antagonist) and FR 139317 (1-10 μM; a selective ET(A) receptor antagonist) prevented initiation of inward currents or enhancement of I(out) by ET-1. The ET(B) receptor agonist tetra-Ala-endothelin-1 (1-20 nM) failed to evoke these responses. Caffeine (10 mM) induced a single transient inward current and prevented any further activation of inward current, or enhancement of I(out), by subsequent application of 16 nM ET-1, suggesting that these currents were mediated by Ca2+ release from internal stores. Rapid intracellular release of Ca2+ by photolysis of nitr-5 activated an inward Cl- current and increased the magnitude of I(out). These results demonstrate the existence of Ca2+ activated C- and K+ channels in pulmonary arterial smooth muscle. The physiological role of these channels is at present uncertain, although their activation may be involved in the contractile responses of pulmonary arterial smooth muscle to ET-1.

Original languageEnglish
Pages (from-to)815-824
Number of pages10
JournalExperimental Physiology
Volume80
Issue number5
Publication statusPublished - 1995

Fingerprint

Calcium-Activated Potassium Channels
Endothelin-1
Smooth Muscle Myocytes
Smooth Muscle
Lung
Photolysis
Patch-Clamp Techniques
Caffeine
Pulmonary Artery
Anions
Ions
nitr 5
FR 139317
bosentan

ASJC Scopus subject areas

  • Physiology

Cite this

Ca2+-activated Cl- and K+ channels and their modulation by endothelin-1 in rat pulmonary arterial smooth muscle cells. / Salter, K. J.; Turner, J. L.; Albarwani, S.; Clapp, L. H.; Kozlowski, R. Z.

In: Experimental Physiology, Vol. 80, No. 5, 1995, p. 815-824.

Research output: Contribution to journalArticle

Salter, K. J. ; Turner, J. L. ; Albarwani, S. ; Clapp, L. H. ; Kozlowski, R. Z. / Ca2+-activated Cl- and K+ channels and their modulation by endothelin-1 in rat pulmonary arterial smooth muscle cells. In: Experimental Physiology. 1995 ; Vol. 80, No. 5. pp. 815-824.
@article{743d9f80e5ac45c19f6d3223e8efa604,
title = "Ca2+-activated Cl- and K+ channels and their modulation by endothelin-1 in rat pulmonary arterial smooth muscle cells",
abstract = "Using the patch-clamp recording technique, we observed that endothelin-1 (ET-1; 0.8-16 nM) enhanced a voltage-activated outward current (I(out)) and induced periodic oscillations of inward current in smooth muscle cells isolated from small pulmonary arteries (200-400 μm in diameter). Anion substitution experiments revealed that the ET-1-induced inward current was carried by Cl- ions. Application of bosentan (10 μM; an ET(A) and ET(B) receptor antagonist) and FR 139317 (1-10 μM; a selective ET(A) receptor antagonist) prevented initiation of inward currents or enhancement of I(out) by ET-1. The ET(B) receptor agonist tetra-Ala-endothelin-1 (1-20 nM) failed to evoke these responses. Caffeine (10 mM) induced a single transient inward current and prevented any further activation of inward current, or enhancement of I(out), by subsequent application of 16 nM ET-1, suggesting that these currents were mediated by Ca2+ release from internal stores. Rapid intracellular release of Ca2+ by photolysis of nitr-5 activated an inward Cl- current and increased the magnitude of I(out). These results demonstrate the existence of Ca2+ activated C- and K+ channels in pulmonary arterial smooth muscle. The physiological role of these channels is at present uncertain, although their activation may be involved in the contractile responses of pulmonary arterial smooth muscle to ET-1.",
author = "Salter, {K. J.} and Turner, {J. L.} and S. Albarwani and Clapp, {L. H.} and Kozlowski, {R. Z.}",
year = "1995",
language = "English",
volume = "80",
pages = "815--824",
journal = "Experimental Physiology",
issn = "0958-0670",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Ca2+-activated Cl- and K+ channels and their modulation by endothelin-1 in rat pulmonary arterial smooth muscle cells

AU - Salter, K. J.

AU - Turner, J. L.

AU - Albarwani, S.

AU - Clapp, L. H.

AU - Kozlowski, R. Z.

PY - 1995

Y1 - 1995

N2 - Using the patch-clamp recording technique, we observed that endothelin-1 (ET-1; 0.8-16 nM) enhanced a voltage-activated outward current (I(out)) and induced periodic oscillations of inward current in smooth muscle cells isolated from small pulmonary arteries (200-400 μm in diameter). Anion substitution experiments revealed that the ET-1-induced inward current was carried by Cl- ions. Application of bosentan (10 μM; an ET(A) and ET(B) receptor antagonist) and FR 139317 (1-10 μM; a selective ET(A) receptor antagonist) prevented initiation of inward currents or enhancement of I(out) by ET-1. The ET(B) receptor agonist tetra-Ala-endothelin-1 (1-20 nM) failed to evoke these responses. Caffeine (10 mM) induced a single transient inward current and prevented any further activation of inward current, or enhancement of I(out), by subsequent application of 16 nM ET-1, suggesting that these currents were mediated by Ca2+ release from internal stores. Rapid intracellular release of Ca2+ by photolysis of nitr-5 activated an inward Cl- current and increased the magnitude of I(out). These results demonstrate the existence of Ca2+ activated C- and K+ channels in pulmonary arterial smooth muscle. The physiological role of these channels is at present uncertain, although their activation may be involved in the contractile responses of pulmonary arterial smooth muscle to ET-1.

AB - Using the patch-clamp recording technique, we observed that endothelin-1 (ET-1; 0.8-16 nM) enhanced a voltage-activated outward current (I(out)) and induced periodic oscillations of inward current in smooth muscle cells isolated from small pulmonary arteries (200-400 μm in diameter). Anion substitution experiments revealed that the ET-1-induced inward current was carried by Cl- ions. Application of bosentan (10 μM; an ET(A) and ET(B) receptor antagonist) and FR 139317 (1-10 μM; a selective ET(A) receptor antagonist) prevented initiation of inward currents or enhancement of I(out) by ET-1. The ET(B) receptor agonist tetra-Ala-endothelin-1 (1-20 nM) failed to evoke these responses. Caffeine (10 mM) induced a single transient inward current and prevented any further activation of inward current, or enhancement of I(out), by subsequent application of 16 nM ET-1, suggesting that these currents were mediated by Ca2+ release from internal stores. Rapid intracellular release of Ca2+ by photolysis of nitr-5 activated an inward Cl- current and increased the magnitude of I(out). These results demonstrate the existence of Ca2+ activated C- and K+ channels in pulmonary arterial smooth muscle. The physiological role of these channels is at present uncertain, although their activation may be involved in the contractile responses of pulmonary arterial smooth muscle to ET-1.

UR - http://www.scopus.com/inward/record.url?scp=0029163137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029163137&partnerID=8YFLogxK

M3 - Article

VL - 80

SP - 815

EP - 824

JO - Experimental Physiology

JF - Experimental Physiology

SN - 0958-0670

IS - 5

ER -