Activation of a large-conductance, ca2+-activated k+ channel by adenosine in porcine coronary arterial smooth muscle

D. K. Bowles, Michael Sturek

Research output: Contribution to journalArticle

Abstract

Adenosine is a hyperpolarizing vasodilator which acts to increase membrane potential by increasing K+ permeablility across the sarcolemma, however the type of K+ channel responsible remains controversial We investigated the effect of adenosine, the A1 receptor agonist R-phenylisopropyladenosine (R-PIA), the A2 agonist CGS 21680 and forskolin, an activator of adenylate cyclase on whole-cell K+ currents in isolated. coronary smooth muscle cells from Yucatan miniature swine. Current-voltage relationships were determined in symmetrical K+ gradients (140K/140K) during ramp depolarizations from -80 mV to +80 mV. Using the amphotericinperforated patch technique, adenosine (10-5 M) increased K+ currents at potentials greater than +10 mV (p <0.05) with no change in the bulk myoplasmic [Ca2+]. Holding currents at -60 mV were unchanged by adenosine. When current noise was low, single channel currents could be resolved. In this condition, adenosine activated a K+ channel with a single channel conductance of ∼ 190 pS which was inhibited by 1 mM TEA. During whole-cell voltage clamp with the pipette solution [Ca2+] clamped at 0 μM (10 mM EGTA), adenosine, R-PIA, CGS 21680 and forskolin all significantly inhibited outward K+ currents. We conclude that adenosine activates a large-conductance Ca2+-activated K+ channel (BK channel), possibly secondary to increases in subsarcolemmal [Ca2+].

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996
Externally publishedYes

Fingerprint

adenosine
smooth muscle
Adenosine
Smooth Muscle
Muscle
Swine
Chemical activation
calcium
swine
Phenylisopropyladenosine
potassium channels
Colforsin
forskolin
agonists
Adenosine A1 Receptor Agonists
Large-Conductance Calcium-Activated Potassium Channels
Miniature Swine
Calcium-Activated Potassium Channels
Sarcolemma
Architectural Accessibility

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

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abstract = "Adenosine is a hyperpolarizing vasodilator which acts to increase membrane potential by increasing K+ permeablility across the sarcolemma, however the type of K+ channel responsible remains controversial We investigated the effect of adenosine, the A1 receptor agonist R-phenylisopropyladenosine (R-PIA), the A2 agonist CGS 21680 and forskolin, an activator of adenylate cyclase on whole-cell K+ currents in isolated. coronary smooth muscle cells from Yucatan miniature swine. Current-voltage relationships were determined in symmetrical K+ gradients (140K/140K) during ramp depolarizations from -80 mV to +80 mV. Using the amphotericinperforated patch technique, adenosine (10-5 M) increased K+ currents at potentials greater than +10 mV (p <0.05) with no change in the bulk myoplasmic [Ca2+]. Holding currents at -60 mV were unchanged by adenosine. When current noise was low, single channel currents could be resolved. In this condition, adenosine activated a K+ channel with a single channel conductance of ∼ 190 pS which was inhibited by 1 mM TEA. During whole-cell voltage clamp with the pipette solution [Ca2+] clamped at 0 μM (10 mM EGTA), adenosine, R-PIA, CGS 21680 and forskolin all significantly inhibited outward K+ currents. We conclude that adenosine activates a large-conductance Ca2+-activated K+ channel (BK channel), possibly secondary to increases in subsarcolemmal [Ca2+].",
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T1 - Activation of a large-conductance, ca2+-activated k+ channel by adenosine in porcine coronary arterial smooth muscle

AU - Bowles, D. K.

AU - Sturek, Michael

PY - 1996

Y1 - 1996

N2 - Adenosine is a hyperpolarizing vasodilator which acts to increase membrane potential by increasing K+ permeablility across the sarcolemma, however the type of K+ channel responsible remains controversial We investigated the effect of adenosine, the A1 receptor agonist R-phenylisopropyladenosine (R-PIA), the A2 agonist CGS 21680 and forskolin, an activator of adenylate cyclase on whole-cell K+ currents in isolated. coronary smooth muscle cells from Yucatan miniature swine. Current-voltage relationships were determined in symmetrical K+ gradients (140K/140K) during ramp depolarizations from -80 mV to +80 mV. Using the amphotericinperforated patch technique, adenosine (10-5 M) increased K+ currents at potentials greater than +10 mV (p <0.05) with no change in the bulk myoplasmic [Ca2+]. Holding currents at -60 mV were unchanged by adenosine. When current noise was low, single channel currents could be resolved. In this condition, adenosine activated a K+ channel with a single channel conductance of ∼ 190 pS which was inhibited by 1 mM TEA. During whole-cell voltage clamp with the pipette solution [Ca2+] clamped at 0 μM (10 mM EGTA), adenosine, R-PIA, CGS 21680 and forskolin all significantly inhibited outward K+ currents. We conclude that adenosine activates a large-conductance Ca2+-activated K+ channel (BK channel), possibly secondary to increases in subsarcolemmal [Ca2+].

AB - Adenosine is a hyperpolarizing vasodilator which acts to increase membrane potential by increasing K+ permeablility across the sarcolemma, however the type of K+ channel responsible remains controversial We investigated the effect of adenosine, the A1 receptor agonist R-phenylisopropyladenosine (R-PIA), the A2 agonist CGS 21680 and forskolin, an activator of adenylate cyclase on whole-cell K+ currents in isolated. coronary smooth muscle cells from Yucatan miniature swine. Current-voltage relationships were determined in symmetrical K+ gradients (140K/140K) during ramp depolarizations from -80 mV to +80 mV. Using the amphotericinperforated patch technique, adenosine (10-5 M) increased K+ currents at potentials greater than +10 mV (p <0.05) with no change in the bulk myoplasmic [Ca2+]. Holding currents at -60 mV were unchanged by adenosine. When current noise was low, single channel currents could be resolved. In this condition, adenosine activated a K+ channel with a single channel conductance of ∼ 190 pS which was inhibited by 1 mM TEA. During whole-cell voltage clamp with the pipette solution [Ca2+] clamped at 0 μM (10 mM EGTA), adenosine, R-PIA, CGS 21680 and forskolin all significantly inhibited outward K+ currents. We conclude that adenosine activates a large-conductance Ca2+-activated K+ channel (BK channel), possibly secondary to increases in subsarcolemmal [Ca2+].

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