Nitric oxide but not prostacyclin is an autocrine endothelial mediator

Henning Schröder, Hans Strobach, Karsten Schrör

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Using porcine aortic endothelial cells, the present study investigates whether stimulation of prostacyclin (PGI2) and nitric oxide also causes elevation of the respective second messengers cAMP and cGMP in the endothelial generator cells. The calcium ionophore A23187 at 0.3-3 μM increased endothelial cGMP levels up to 27-fold in an l-arginine-dependent manner as assessed through complete inhibition by NG-monomethyl-l-arginine (100μM). The 36-fold PGI2 stimulation by 3μM A23187 was not accompanied by an intracellular increase in cAMP or an enhanced cAMP efflux. Correspondingly, the PGI2 mimetic iloprost (10 pM-100 μM) did not change endothelial cAMP levels. However, forskolin (1-100 μM) and prostaglandin E2 (PGE2) (0.1-10 μM) produced concentration-dependent increases in cAMP with a 9-fold and 8-fold stimulation at 100 μM forskolin and 10μM PGE2, respectively. These results demonstrate that in contrast to NO, PGI2 acts as a strictly paracrine hormone without affecting the respective second messenger cAMP in the endothelial generator cells.

Original languageEnglish (US)
Pages (from-to)533-537
Number of pages5
JournalBiochemical Pharmacology
Volume43
Issue number3
DOIs
StatePublished - Feb 4 1992
Externally publishedYes

Bibliographical note

Funding Information:
Acknowledgements-The authorst hankC hristineM achun-sky for expertt echnicala ssistancea nd Erika Lohmannf or competents upporti n the preparationo f this manuscript. This work was supported in part by the Deutsche Fo~hungs~meinscha~( Schr 194/7-4).

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