Abstract
K+ channels which are inhibited by intracellular ATP (ATPi) (KATP channels) are thought to be the physiological target site of the K+ channel opening drugs (2) and to underlie a variety of physiological phenomena including hypoxia induced vasodilation (3). However, electrophysiological evidence for ATPi-regulated K+ currents in smooth muscle is scarce. We, therefore, investigated the effects of one K+ channel opener, lemakalim, and metabolic inhibition on the membrane conductance of freshly dissociated rabbit mesenteric artery smooth muscle cells, using the perforated-patch whole cell recording technique (6). The cells were metabolically inhibited with 1 mM iodoacetic acid and 50 μM dinitrophenol. Both lemakalim (0.1-3 μM) and metabolic inhibition activated a time-independent and glyburide sensitive K+ current at physiological membrane potentials. The similarities between the lemakalim and metabolic inhibition activated currents suggest that a single class of channels underlies both currents. These results are the first whole-cell current recordings to demonstrate the activation of a smooth muscle membrane conductance by metabolic inhibition, lending support to the view that hypoxia induced vasodilation arises from the activation of KATP channels.
Original language | English |
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Pages (from-to) | 118-120 |
Number of pages | 3 |
Journal | Pflugers Archiv European Journal of Physiology |
Volume | 420 |
Issue number | 1 |
DOIs | |
State | Published - 1 Jan 1992 |
Externally published | Yes |
Keywords
- K current
- metabolic inhibition
- smooth muscle
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Physiology (medical)