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Last Updated: 3 years ago

Possible Interaction: Adenosine and Epoprostenol

supplement:

Adenosine

Research Papers that Mention the Interaction

Seven of the eight patients who had minimal pulmonary vasodilation in response to adenosine (mean reduction in resistance units, <20 percent) still had a significant reduction in pulmonary vascular resistance when treated with epoprostenol (mean, 39+/-14 percent; P=0.002).
The long-term effects of epoprostenol exceeded the short-term pulmonary vasodilator response to adenosine in all but one patient.
The New England journal of medicine  •  1998  |  View Paper
The addition of adenosine to microvascular endothelial cells induced an increase in NO and prostacyclin levels.
These findings provide novel insight into the role of adenosine in skeletal muscle blood flow regulation and vascular function by revealing that both interstitial and plasma adenosine have a stimulatory effect on NO and prostacyclin formation.
Hypertension  •  2010  |  View Paper
Prostacyclin plays an important cardioprotective role for the ischemic heart, having antiplatelet and antifibrillatory effects, potentiates the antiplatelet effect of the nitrovasodilators and nitric oxide, and increases the release of adenosine.
Zeitschrift fur Kardiologie  •  1995  |  View Paper
Furosemide, prostaglandins (PGE2 and PGI2 ) and adenosine modulate its function. (
Nihon Naibunpi Gakkai zasshi  •  1992  |  View Paper
Prostacyclin inhibits platelet aggregation by stimulating adenylate cyclase, leading to an increase in adenosine 3’ : 5‘-cyclic monophosphate (cyclic AMP) levels in the platelets [5, 61.
Clinical science  •  1981  |  View Paper
Using platelet-rich plasma, we examined the effect of Increasing concentrations of ethanol (0.05% to 1.0%) on the platelet-Inhibitory effects of a submaxlmal dose (5 × 10−10 M) of prostacyclin , the concomitant production of cyclic 3′,5′- adenoslne monophosphate (AMP), and the release of thromboxane A2.
Arteriosclerosis  •  1988  |  View Paper
Adenosine also significantly attenuated the renin release response to PGI2.
We conclude that adenosine can inhibit the renin release response to both renal artery hypotension and PGI2 and that this effect is most likely mediated by a direct action of adenosine on juxtaglomerular cells.
Naunyn-Schmiedeberg's Archives of Pharmacology  •  2004  |  View Paper
This data suggest that PKC and PGI2 regulate the direct negative inotropic effect of adenosine , which is abolished during ischemia.
Prostaglandins, leukotrienes, and essential fatty acids  •  2000  |  View Paper
These results suggest that after myocardial ischemia prostacyclin has an inhibitory effect on adenosine release.
European journal of pharmacology  •  1999  |  View Paper
It is concluded that adenosine and PGI2 counteract hypoxia‐induced increases in pulmonary vascular resistance similarly, but the reduction in pulmonary artery pressure was greater with PGI2 at infusion rates, causing minor systemic haemodynamic changes.
Acta anaesthesiologica Scandinavica  •  1991  |  View Paper
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