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Published on: June 18, 2012
Peroxynitrite induces arteriolar smooth muscle cells membrane hyperpolarization with arteriolar hyporeactivity in
Bing-Xing Pan1, Gui-Ling Zhao, Xu-Liang Huang
1Key Lab for Shock and Microcirculation of PLA, Department of Pathophysiology, The First Military Medical University, Guangzhou 510515, PR China.
Abstract:
Peroxynitrite (ONOO-) has been recently known to act as a potent cytotoxin during pathogenesis of various diseases. This study aimed to investigate the possible effect of ONOO- on the cremaster muscle arteriolar reactivity in response to noradrenaline and subsequently determined whether membrane hyperpolarization and potassium channel activation were involved in ONOO(-)-induced alteration of arteriolar reactivity. The results demonstrated that 1) ONOO- could decrease arteriolar reactivity in a time- and concentration-dependent manner with no significant alteration of arteriolar diameter; 2) Superfusion with 20 microM ONOO- over 40 minutes showed slight but not significant influence on the resting potential (Em) of arteriolar smooth muscle cells (ASMCs). However, ASMCs subjected to 50 or 100 microM ONOO- administration were significantly hyperpolarized. As control, treatment with 50 microM decomposed ONOO- or Kreb's solution had little effect on the Em of ASMCs; 3) ONOO(-)-induced arteriolar hyporeactivity could be greatly reversed by co-administration of KCl and partially by TEA. The above results indicated that membrane hyperpolarization and potassium channel activation were preferentially responsible for the reduction of cremaster muscle arteriolar reactivity after exposure to ONOO-.
Insights
Peroxynitrite (ONOO-) reduces cremaster muscle arteriolar reactivity by causing membrane hyperpolarization and activating potassium channels. This finding is crucial for understanding disease pathogenesis involving ONOO-.
Area of Science:
- Physiology
- Pathophysiology
- Vascular Biology
Background:
- Peroxynitrite (ONOO-) is recognized as a significant cytotoxin implicated in the pathogenesis of various diseases.
- Understanding the vascular effects of ONOO- is crucial for developing therapeutic strategies.
- Arteriolar reactivity plays a key role in regulating blood flow and tissue perfusion.
Purpose of the Study:
- To investigate the impact of ONOO- on cremaster muscle arteriolar reactivity.
- To determine the role of membrane hyperpolarization and potassium channel activation in ONOO(-)-induced changes in arteriolar reactivity.
Main Methods:
- Exposure of cremaster muscle arterioles to varying concentrations and durations of ONOO-.
- Measurement of arteriolar diameter and reactivity to noradrenaline.
- Assessment of arteriolar smooth muscle cell membrane potential (Em) using microelectrode techniques.
- Evaluation of the effects of potassium channel blockers (TEA) and KCl on ONOO(-)-induced hyporeactivity.
Main Results:
- ONOO- significantly decreased arteriolar reactivity in a time- and concentration-dependent manner without altering basal diameter.
- Higher concentrations of ONOO- (50-100 microM) induced significant hyperpolarization of arteriolar smooth muscle cells.
- ONOO(-)-induced hyporeactivity was reversed by KCl and partially by tetraethylammonium (TEA), indicating potassium channel involvement.
Conclusions:
- Peroxynitrite impairs cremaster muscle arteriolar function.
- Membrane hyperpolarization and subsequent potassium channel activation are key mechanisms underlying ONOO(-)-induced arteriolar hyporeactivity.
- These findings provide insights into the vascular pathophysiology associated with diseases involving elevated peroxynitrite levels.
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