Abstract
The angiotensin converting enzyme (ACE) inhibitor perindoprilat evokes endothelium-dependent relaxations in perfused isolated canine arteries. Kininogens, the precursors of bradykinin, elicit endothelium-dependent relaxations which are potentiated by perindoprilat, inhibited by B2-kinin antagonists and partially impaired after inhibition of NO synthase. These observations suggest that locally produced kinins may stimulate the production of NO and endothelium-derived hyperpolarizing factor, and that this action is potentiated by ACE inhibitors.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Angiotensin-Converting Enzyme Inhibitors / pharmacology*
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Animals
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Arginine / analogs & derivatives
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Arginine / pharmacology
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Bradykinin / analogs & derivatives
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Bradykinin / antagonists & inhibitors
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Bradykinin / pharmacology*
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Carotid Arteries / drug effects
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Carotid Arteries / metabolism
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Carotid Arteries / physiology*
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Dogs
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Endothelium, Vascular / physiology*
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In Vitro Techniques
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Indoles / pharmacology*
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Indomethacin / pharmacology
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Kininogens / pharmacology*
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Kinins / metabolism*
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / metabolism
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Muscle, Smooth, Vascular / physiology*
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Nitroarginine
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Nitroprusside / pharmacology
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Vasodilation / drug effects
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Vasodilation / physiology*
Substances
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Angiotensin-Converting Enzyme Inhibitors
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Indoles
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Kininogens
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Kinins
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bradykinin, des-Arg(9)-
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Nitroprusside
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Nitroarginine
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perindoprilat
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bradykinin, Leu(8)-des-Arg(9)-
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Arginine
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NPC 567
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Bradykinin
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Indomethacin