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Modulation of K+ and Ca2+ channels by histamine H1‐receptor stimulation in rabbit coronary artery cells.
Author(s) -
Ishikawa T,
Hume J R,
Keef K D
Publication year - 1993
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1993.sp019777
Subject(s) - ryanodine receptor , tetraethylammonium , thapsigargin , histamine , chemistry , patch clamp , biophysics , membrane potential , medicine , extracellular , stimulation , agonist , endocrinology , nicardipine , cyclopiazonic acid , caffeine , intracellular , electrophysiology , calcium , receptor , biology , potassium , biochemistry , organic chemistry
1. The modulation of whole‐cell K+ and Ca2+ currents by stimulation of histamine H1‐receptors in freshly isolated single smooth muscle cells from the rabbit coronary artery was characterized using the patch‐clamp technique at 35 degrees C. Single‐channel K+ currents were also analysed using the cell‐attached patch configuration. 2. The histamine H1‐receptor agonist, 2‐(2‐aminoethyl)pyridine (AEP) (0.1 mM), increased the amplitude of voltage‐activated inward Ba2+ currents, recorded using the perforated‐patch recording technique, which could be completely blocked by the dihydropyridine antagonist, nicardipine (1 microM). 3. Whole‐cell outward K+ currents in rabbit coronary artery cells could be classified into at least two components: (a) a slowly inactivating, 4‐aminopyridine (4‐AP)‐sensitive low‐noise current, and (b) a non‐inactivating, tetraethylammonium (TEA)‐sensitive high‐noise current. 4. AEP (0.1 mM) caused changes in whole‐cell outward K+ currents which depended upon membrane voltage. Specifically: (a) AEP enhanced the amplitude of outward currents at voltages between ‐30 and 0 mV, and (b) AEP decreased the outward currents at more positive potentials. 5. The removal of extracellular Ca2+ caused little inhibition of the effects of AEP on K+ currents, whereas the depletion of intracellular Ca2+ stores by pretreatment with ryanodine and caffeine prevented the effects of AEP on K+ channels. Moreover, acute exposure to ryanodine (10 microM) or thapsigargin (1 microM), a Ca(2+)‐ATPase inhibitor, caused voltage‐dependent changes in the outward currents similar to those observed with AEP. These results suggest that the voltage‐dependent effects of AEP on K+ currents are mainly mediated by release of Ca2+ from intracellular stores. 6. The dual stimulatory and inhibitory effect of AEP on whole‐cell K+ currents was shown to be due to a differential effect on two distinct types of K+ channels. The stimulatory effect observed over the voltage range ‐30 to 0 mV was prevented by pretreatment of cells with low concentrations of TEA (1 mM), whereas the inhibitory effect observed at positive potentials was prevented by pretreatment of cells with 4‐AP (3 mM). 7. Single‐channel recordings revealed two types of unitary K+ currents with conductances of 225 and 70 pS in the cell‐attached configuration with symmetrical K+ solutions (150 mM K+ in pipette‐150 mM K+ in bath). Bath application of AEP (0.1 mM) caused a marked increase in the open probability of the large conductance channels.(ABSTRACT TRUNCATED AT 400 WORDS)