Abstract
Effects of chronic nicotine treatment on the relative levels of expression of Na,K-ATPase alpha and beta subunit isoforms were determined in rat cerebral microvessels and capillary-depleted brain homogenates by Western blot analysis. Nicotine, 4.5 mg/kg/day, was administered s.c. by osmotic mini-pumps for 14 days. Expression of alpha 2 isoform in microvessels and brains of nicotine-treated rats was reduced to 0.26 and 0.58 of control levels, respectively. Expression of alpha 1, alpha 3, beta 1 or beta 2 was unchanged. Nicotine decreased cerebromicrovascular and brain Na,ATPase enzymatic activities by 22% and 17%, respectively. It is suggested that chronic exposure to nicotine reduces expression of functional Na,K-ATPase at the blood-brain barrier and brain by downregulating the alpha 2 isoform.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Arterioles / drug effects
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Arterioles / enzymology
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / physiology*
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Brain / drug effects
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Brain / enzymology*
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Capillaries / drug effects
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Capillaries / enzymology
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Cerebrovascular Circulation*
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Female
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Gene Expression
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Isoenzymes / biosynthesis
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Isoenzymes / isolation & purification
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Isoenzymes / metabolism*
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Male
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Microcirculation / drug effects
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Microcirculation / enzymology*
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / enzymology
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Nicotine / pharmacology*
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Rats
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Rats, Sprague-Dawley
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Sodium-Potassium-Exchanging ATPase / biosynthesis
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Sodium-Potassium-Exchanging ATPase / isolation & purification
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Sodium-Potassium-Exchanging ATPase / metabolism*
Substances
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Isoenzymes
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Nicotine
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Sodium-Potassium-Exchanging ATPase