Abstract
The effects of human urotensin II on coronary flow were studied in the perfused rat heart. Urotensin II transiently decreased coronary flow, then induced sustained vasodilatation. In the presence of a cyclooxygenase inhibitor, diclofenac, coronary vasodilatation was significantly inhibited. A nitric oxide synthase inhibitor, N(G)-nitro-L-arginine (L-NNA), attenuated the urotensin-induced vasodilatation. These data suggest that urotensin II modulates coronary flow through factors such as cyclooxygenase products and nitric oxide to elicit coronary vasodilatation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Coronary Vessels / drug effects*
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Diclofenac / pharmacology
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Enzyme Inhibitors / pharmacology
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Humans
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In Vitro Techniques
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Male
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase Type III
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Nitroarginine / pharmacology
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Rats
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Rats, Inbred F344
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Urotensins / antagonists & inhibitors
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Urotensins / pharmacology*
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Vasoconstrictor Agents / pharmacology*
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Vasodilator Agents / pharmacology*
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Enzyme Inhibitors
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Urotensins
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Vasoconstrictor Agents
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Vasodilator Agents
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Diclofenac
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Nitroarginine
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urotensin II
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NOS3 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type III
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Nos3 protein, rat