Abstract
Cromakalim, pinacidil and nitroprusside provoked concentration-dependent relaxations of K(+)-depolarized rat aortae. Glibenclamide, tolbutamide and to a lesser extent tetraethylammonium antagonized the vasorelaxant action of cromakalim and pinacidil. Cromakalim, pinacidil but not nitroprusside elicited a marked increase in 86Rb outflow from preloaded and perifused aortic rings. These increases in 86Rb outflow were inhibited in a concentration-dependent manner by glibenclamide and tetraethylammonium. Our data extend previous observations indicating the involvement of K+ channels in the vasorelaxant properties of cromakalim and pinacidil. Moreover, the present findings suggest that both compounds could interfere with a vascular type of ATP-sensitive K+ channels.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aorta, Thoracic / drug effects
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Aorta, Thoracic / metabolism
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Benzopyrans / antagonists & inhibitors*
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Cromakalim
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Glyburide / pharmacology
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Guanidines / antagonists & inhibitors*
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Hypoglycemic Agents / pharmacology*
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In Vitro Techniques
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Muscle Contraction / drug effects
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Muscle Relaxation / drug effects
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / metabolism*
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Nitroprusside / pharmacology
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Parasympatholytics / pharmacology
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Pinacidil
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Potassium Channels / drug effects
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Pyrroles / antagonists & inhibitors*
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Rats
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Rats, Inbred Strains
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Rubidium Radioisotopes
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Sulfonylurea Compounds / pharmacology*
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Tetraethylammonium Compounds / pharmacology
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Tolbutamide / pharmacology
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Vasodilator Agents / pharmacology
Substances
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Benzopyrans
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Guanidines
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Hypoglycemic Agents
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Parasympatholytics
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Potassium Channels
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Pyrroles
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Rubidium Radioisotopes
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Sulfonylurea Compounds
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Tetraethylammonium Compounds
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Vasodilator Agents
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Cromakalim
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Nitroprusside
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Pinacidil
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Tolbutamide
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Glyburide