Abstract
Long-term (24 h) pretreatment of cultured rat vascular smooth muscle cells with 100 nM angiotensin and 1 microM vasopressin induced a marked reduction of the maximal binding capacity of atrial natriuretic peptide (ANP) receptors in a fashion similar to that induced by phorbol ester. The down-regulation of the receptors induced by vasoconstrictors and phorbol ester was concomitantly associated with an attenuation of ANP-stimulated cGMP accumulation. These data suggest that vasoconstrictor-induced activation of protein kinase C is involved in the mechanism of heterologous down-regulation of vascular ANP receptors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiotensin II / physiology
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Animals
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Arginine Vasopressin / physiology
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Cyclic GMP / metabolism
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Humans
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In Vitro Techniques
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Iodine Radioisotopes
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / metabolism
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Piperidines / metabolism
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Rats
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Receptors, Atrial Natriuretic Factor
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Receptors, Cell Surface / physiology*
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Tetradecanoylphorbol Acetate / pharmacology
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Vasoconstrictor Agents / pharmacology*
Substances
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Iodine Radioisotopes
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Piperidines
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Receptors, Cell Surface
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Vasoconstrictor Agents
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Angiotensin II
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Arginine Vasopressin
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preclamol
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Receptors, Atrial Natriuretic Factor
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Cyclic GMP
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Tetradecanoylphorbol Acetate