Abstract
We examined the role of endothelium-derived relaxing factors nitric oxide (NO), endothelium-derived hyperpolarising factor (EDHF), and prostaglandins (PGs) to P(2Y1)- and P(2Y2)-purinoceptor-induced vasodilation in isolated rat kidney. To do it, we analysed the renal response to ATP, 2-methylthio ATP, and UTP in rat renal vasculature under normal conditions and after the administration of: N(w)-nitro-L-arginine (L-NAME), increased K(+) concentration, indomethacin, and L-NAME and increased K(+) together. Our results indicate that the vasodilator response to P(2Y1)- and P(2Y2)-purinoceptor activation in the isolated perfused kidney of rats is subserved by EDHF and NO.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Biological Factors / pharmacology
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Dose-Response Relationship, Drug
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In Vitro Techniques
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Kidney / blood supply
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Kidney / drug effects
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Kidney / physiology*
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Male
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Nitric Oxide / pharmacology
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Nitric Oxide / physiology*
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Perfusion
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Prostaglandins / pharmacology
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Rats
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Rats, Wistar
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Receptors, Purinergic P2 / physiology*
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Receptors, Purinergic P2Y1
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Receptors, Purinergic P2Y2
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Vasodilation / drug effects
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Vasodilation / physiology*
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Vasodilator Agents / pharmacology*
Substances
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Biological Factors
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P2ry1 protein, rat
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P2ry2 protein, rat
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Prostaglandins
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Receptors, Purinergic P2
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Receptors, Purinergic P2Y1
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Receptors, Purinergic P2Y2
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Vasodilator Agents
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endothelium-dependent hyperpolarization factor
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Nitric Oxide