Effects of amiloride analogues on the production of prostacyclin by aortic endothelial cells

British Journal of Pharmacology
J M BoeynaemsE J Cragoe

Abstract

1. The release of prostacyclin (PGI2) from bovine aortic endothelial cells stimulated by adenosine 5'-triphosphate (ATP) was decreased by amiloride analogues bearing alkyl groups on the 5-amino nitrogen atom, like 5-(N-ethyl-N-isopropyl)amiloride (EIPA), which are inhibitors of the Na+/H+ exchanger. Analogues substituted on a terminal guanidino nitrogen atom were not inhibitory. 2. The release of PGI2 induced by ATP was not significantly depressed in a Na+-poor medium or in a medium acidified to pH 6.9, two conditions known to inhibit the Na+/H+ exchanger. 3. Cytoplasmic alkalinization by ammonium chloride did not suppress the inhibitory action of EIPA. By itself, ammonium chloride decreased the response of endothelial cells to ionophore A23187 and ATP, whereas sodium acetate had no effect. 4. EIPA did not decrease the mobilization of free arachidonic acid induced by ATP. It inhibited the conversion of exogenous arachidonate into PGI2 and prostaglandin E2 (PGE2). 5. Although the intracellular pH was not measured in this study, it seems unlikely that cytoplasmic alkalinization via the activation of the Na+/H+ exchanger plays a significant role in the stimulatory action of ATP on the release of PGI2 from endothelial cells. The in...Continue Reading

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Citations

Jan 1, 1990·Trends in Pharmacological Sciences·J M Boeynaems, J D Pearson
Mar 25, 1991·Biochemical and Biophysical Research Communications·B BattistiniP Sirois

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