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Discover Supplement-Drug Interactions

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Last Updated: 8 months ago

Possible Interaction: Epoprostenol and Calcium Supplement

Research Papers that Mention the Interaction

Both are strongly reduced if Ca2+ addition is preceded by SNP or PGI2.
The Biochemical journal  •  1994  |  View Paper
One of them, cAMP regulation, is coupled with a potent inhibiting effect of prostacyclin , an adenylate cyclase activator, on Ca2+in increase in stimulated neutrophils.
Biokhimiia  •  1988  |  View Paper
A low-dose infusion of calcium or norepinephrine (known stimulants of prostacyclin) increased renal prostacyclin release in normal subjects and controls with renal insufficiency.
The New England journal of medicine  •  1986  |  View Paper
Ca++ can stimulate prostaglandin E2 (PGE2) and/or prostacyclin (PGI2) release in vitro, which may modulate Ca++ vascular effects.
The Journal of clinical investigation  •  1986  |  View Paper
alpha 2-Adrenoceptor stimulation in platelets showed an increased sensitivity to adrenaline, as determined by sensitivity in counteracting the inhibitor effect of PGI2 on intracellular free calcium concentration in untreated patients with essential hypertension, when compared with treated patients or normotensive subjects.
Clinical science  •  1985  |  View Paper
Therefore, it is probable that calcium ions and calcium-activated calmodulin play a role in the effect of prostacyclin.
Journal of Physiology-Paris  •  1999  |  View Paper
P uterine artery prostacyclin production increased similarly with ANG II (61%) and A23187 (78%) in the presence of calcium (2 mM), whereas NP uterine arteries responded only to A23187 (71%).
Endocrinology  •  1993  |  View Paper
In this preparation PGI2 increased the calcium current in a concentration-dependent manner, by up to 60% over the control value (at 10 microM), whereas PGE1 (tested in the range 1 nM-10 microM) had practically no effect on the calcium current.
PGI2 (tested in the range 1 nM-10 microM) had marked effects on both action potential and calcium current.
These data indicate that the positive inotropic effect exerted by PGI2 on cardiac preparations is probably due to enhancement in the calcium current via a cAMP-dependent phosphorylation of the calcium channel.
Journal of molecular and cellular cardiology  •  1991  |  View Paper
Application of PGI2 reduced the depth of ischemia-evoked drop of Ca2+e by 50% without accelerating recovery during recirculation; the post-ischemic increase of BBB permeability to fluorescein was also diminished.
Acta neurobiologiae experimentalis  •  1990  |  View Paper
Moreover myocardial intracellular calcium availability seems to be influenced by PGI2.
Prostaglandins, leukotrienes, and essential fatty acids  •  1988  |  View Paper
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