Intracellular Regulation of the Synthesis of the Vascular Antiaggregating Agent : Prostacyclin

Larrue, J; Dorian, B.; Daret, Danièle; Demond-Henri, J.; Bricaud, H

doi:10.1093/eurheartj/4.suppl_b.17-a

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“…As shown on Figs. 3 and 4, the responses to ionophore A23 187 and arachidonic acid were also lost in strips of deendothelialized aorta obtained either by rubbing or by scraping. The 30-fold stimulation of 6-K-PGFia output by ionophore A23187 (5 MM) in the intact rabbit aorta was reduced to 1.3-fold in deendothelialized strips (mean of eight experiments).…”

Section: Resultsmentioning

confidence: 95%

“…PGI2 is the major eicosanoid produced by cultured smooth muscle cells from rat (1), rabbit (2,3), and bovine (4-6) aorta, whereas smooth muscle cells from porcine aorta synthesize mainly prostaglandins E2 (PGE2) Fl,; PGE2, prostaglandin E2; PGF2,., prostaglandin F2l,; PG12, prostacyclin; RPHPLC, reversed-phase high performance liquid chromatography.…”

Section: Introductionmentioning

confidence: 99%

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Prostacyclin production by the deendothelialized rabbit aorta.

Boeynaems¹,

Galand²,

Ketelbant³

1985

J. Clin. Invest.

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The acute effect of in vitro deendothelialization on the production of prostacyclin (PG12) by the rabbit aorta has been investigated. The effectiveness of removing endothelium by rubbing it against filter paper or scraping it with a scalpel was demonstrated by scanning electron microscopy and en face examination after silver staining. Endothelium removal produced an immediate stimulation of PGI2 release, resulting in 408% of the control after rubbing and 367% of the control after scraping, during the first 30-min period of incubation. This increased production of PG12 gradually declined over time to reach values similar to the control after 2 h. At that time, the deendothelialized aorta was totally unresponsive to the stimuli that increase PG12 release in the intact aorta (acetylcholine, ADP, ionophore A23187, and arachidonic acid). The enhanced production of PG12 in the deendothelialized aorta was associated with an increased release of free arachidonic acid (353% of the control): in contrast with PG12, this stimulation was maintained for at least 150 min. A transient exposure of the deendothelialized aorta to ibuprofen (250 1M) was followed by a rebound of PG12 production, which was also prolonged by BW-755C (3-10 ;&M). In conclusion, removal of the endothelium triggered an immediate and sustained mobilization of free arachidonic acid in the rabbit aorta: the resulting increase of P012 production was short-lived, probably as a consequence of cyclooxygenase self-inactivation. Our results indicate that the subendothelium has a significant capacity to produce PGI2, but that this capacity is expressed only briefly.

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Section: Resultsmentioning

confidence: 95%