Endothelin/sarafotoxin receptor induced phosphoinositide turnover: effects of pertussis and cholera toxins and of phorbol ester.

Abstract

The induction of phosphoinositide hydrolysis (PI) by endothelin/sarafotoxin (ET/SRTX) receptors in rat heart myocytes was investigated by the use of bacterial toxins as well as a phorbol ester. Both pertussis- and choleratoxin enhanced the stimulation of PI hydrolysis. Phorbol ester treatment of the myocytes for short periods distinguished between two types of PI-hydrolysis, the one induced by endothelins and the other by sarafotoxins. The possible mediation of G-protein (s) in the induction by ET/SRTX receptors of PI-hydrolysis is discussed.

• Authors: R Galron, A Bdolah, Y Kloog, M Sokolovsky
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 171 Issue 3 Pg. 949-54 (Sep 28 1990) ISSN: 0006-291X [Print] United States
• PMID: 2171512 (Publication Type: Journal Article)

Chemical References

• Endothelins
• Phosphatidylinositols
• Receptors, Cell Surface
• Receptors, Cholinergic
• Receptors, Endothelin
• Receptors, Peptide
• Vasoconstrictor Agents
• Viper Venoms
• Virulence Factors, Bordetella
• sarafotoxin receptor
• sarafotoxins s6
• Inositol
• Cholera Toxin
• Tetradecanoylphorbol Acetate

Topics

• Animals
• Animals, Newborn
• Cells, Cultured
• Cholera Toxin (pharmacology)
• Endothelins (pharmacology)
• Heart (drug effects)
• Inositol (metabolism)
• Myocardium (metabolism)
• Phosphatidylinositols (metabolism)
• Rats
• Receptors, Cell Surface (drug effects, physiology)
• Receptors, Cholinergic (drug effects, physiology)
• Receptors, Endothelin
• Receptors, Peptide
• Tetradecanoylphorbol Acetate (pharmacology)
• Vasoconstrictor Agents (pharmacology)
• Viper Venoms (pharmacology)
• Virulence Factors, Bordetella (pharmacology)