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Intracellular divalent cations block smooth muscle K+ channels
C H Gelband1, T Ishikawa, J M Post
1Department of Physiology, University of Nevada School of Medicine, Reno 89557-0046.
Circulation Research
|July 1, 1993
Summary
Delayed rectifier potassium channels (IK(dr)) in smooth muscle are sensitive to intracellular magnesium (Mg2+) and calcium (Ca2+). These cations regulate channel activity, impacting cell membrane potential and smooth muscle contraction.
Area of Science:
- Physiology
- Molecular Biology
- Cardiovascular Research
Background:
- Delayed rectifier potassium currents (IK(dr)) are crucial for regulating membrane potential in smooth muscle cells.
- Intracellular divalent cations, particularly magnesium (Mg2+) and calcium (Ca2+), are known to influence ion channel function.
- Understanding the modulation of IK(dr) by these cations is essential for comprehending smooth muscle physiology and pathophysiology.
Purpose of the Study:
- To investigate the sensitivity of delayed rectifier K+ channels to intracellular Mg2+ and Ca2+ in various smooth muscle cell types.
- To elucidate the impact of Mg2+ and Ca2+ on the biophysical properties and function of IK(dr).
- To determine how these cation-dependent modulations affect smooth muscle cell membrane potential and contractility.
Main Methods:
- Utilized the patch-clamp technique, including whole-cell voltage-clamp and inside-out patch recordings.
- Examined IK(dr) in renal, pulmonary, coronary, and colonic smooth muscle cells.
- Manipulated intracellular Mg2+ and Ca2+ concentrations and assessed their effects on channel activity and kinetics.
Main Results:
- A 4-aminopyridine (4-AP)-sensitive IK(dr) was identified across multiple smooth muscle types.
- Increased intracellular Mg2+ significantly reduced 4-AP-sensitive IK(dr) in all cell types studied.
- Elevated intracellular Ca2+ (induced by H1 receptor agonist or ryanodine) also decreased IK(dr), mimicking Mg2+ effects.
- Mg2+ reduced the open probability of a specific K+ channel (59 ± 10 pS) in a concentration- and voltage-dependent manner, primarily by decreasing mean open time.
Conclusions:
- A 4-AP-sensitive delayed rectifier K+ channel in vascular and visceral smooth muscle is modulated by intracellular Mg2+ and Ca2+.
- Changes in intracellular divalent cation concentrations can alter IK(dr) function, influencing membrane potential.
- These modulations by Mg2+ and Ca2+ likely play a significant role in regulating smooth muscle contractility.