Abstract
We analyzed the effects of hypoxia and reoxygenation on changes in contractile activity in rat aortic smooth muscles. Both hypoxia and reoxygenation induced relaxation of smooth muscle cells precontracted with high-potassium Krebs solution (30 mM KCl) or α1-adrenoceptor agonist phenylephrine. Vasodilation resulted from enhancement of potassium permeability of smooth muscle cell membranes caused by activation of voltage-gated potassium channels (triggered by both precontracting agents) or by opening of ATP-sensitive potassium channels (phenylephrine). In isolated smooth muscle cells, both hypoxia and inhibition of Na+,K+-ATPase with ouabain led to depletion of intracellular store of macroergic substances, reduced potassium concentration, and elevated the content of sodium ions.
Keywords:
hypoxia; rat aorta; reoxygenation, Na+,K+-ATPase; smooth muscle cells.
MeSH terms
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Adenosine Triphosphate / metabolism
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Adrenergic alpha-1 Receptor Agonists / pharmacology
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Animals
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Aorta / cytology
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Aorta / drug effects
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Aorta / metabolism
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Enzyme Inhibitors / pharmacology
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Hypoxia / metabolism*
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Isometric Contraction / drug effects*
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KATP Channels / metabolism
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Male
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / metabolism
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Myocytes, Smooth Muscle / cytology
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Myocytes, Smooth Muscle / drug effects
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Myocytes, Smooth Muscle / metabolism
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Ouabain / pharmacology
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Oxygen / pharmacology*
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Phenylephrine / pharmacology
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Potassium / metabolism*
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Potassium Channels, Voltage-Gated / metabolism
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Primary Cell Culture
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Rats
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Rats, Wistar
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Sodium / metabolism*
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Sodium-Potassium-Exchanging ATPase / metabolism
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Tissue Culture Techniques
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Vasodilation / drug effects
Substances
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Adrenergic alpha-1 Receptor Agonists
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Enzyme Inhibitors
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KATP Channels
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Potassium Channels, Voltage-Gated
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Phenylephrine
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Ouabain
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Adenosine Triphosphate
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Sodium
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Sodium-Potassium-Exchanging ATPase
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Potassium
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Oxygen