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

D. K. Bowles, M. Sturek

Research output: Contribution to journalArticlepeer-review


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)
Pages (from-to)A70
JournalFASEB Journal
Issue number3
StatePublished - Dec 1 1996
Externally publishedYes

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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