6-Ketoprostaglandin E1 stimulation of rat and rabbit renal adenylate cyclase-cyclic AMP systems.

@article{Rapp19816KetoprostaglandinES,
  title={6-Ketoprostaglandin E1 stimulation of rat and rabbit renal adenylate cyclase-cyclic AMP systems.},
  author={N. S. Rapp and T. Zenser and B. Davis},
  journal={Biochimica et biophysica acta},
  year={1981},
  volume={673 2},
  pages={
          163-9
        }
}
6-Ketoprostaglandin E1 effects on rat and rabbit renal adenylate cyclase-cyclic AMP systems were examined. Adenylate cyclase activity was assessed in the 1000 X g fractions prepared from different areas of kidney. 6-Ketoprostaglandin E1 caused a dose-dependent increase in rat cortical and medullary adenylate cyclase activity with 8 x 10(-6) M being the lowest effective concentration. Combinations of maximal stimulatory concentrations of 6-ketoprostaglandin E1 and prostaglandin I2 caused… 
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11 Citations

11 Citations

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Citation Type

Prostaglandin‐Related Renin Release from Rabbit Renal Cortical Slices
TLDR
The results lend further support to the concept that 6-keto- PGE1 is capable of releasing renin through a direct action as well as inactivation of PGI2 and platelet antiaggregatory activity.
Biochemical evidence for PGI2 and PGE2 receptors in the rabbit renal preglomerular microvasculature.
Prostaglandin-related renin release from rabbit renal cortical slices.
TLDR
The results lend further support to the concept that 6-keto PgE1 is capable of releasing renin through a direct action, as well as inactivation of PGI2 and platelet antiaggregatory activity as an index of stability.
Prostacyclin modulates cholesteryl ester hydrolytic activity by its effect on cyclic adenosine monophosphate in rabbit aortic smooth muscle cells.
TLDR
Results suggest that increased synthesis of PGI2 by neointimal SMC in the injured aortic wall may, at least in part, explain the changes in CE catabolism and accumulation following injury.
6-Keto-Prostaglandin E1: Biosynthesis and Circulatory Effects
The changes in circulatory function induced by 6-keto-prostaglandin E1 (6-keto-PGE1) bear a close resemblance to the changes caused by prostacyclin (PGI2). Like PGI2, 6-keto-PGE1 is potent in…
Cardiovascular Responses to 6-Keto-PGE1, a Potent Renin-Releasing Agent
A remarkable range of circulatory effects has been attributed to prostacyclin (PGI2). These include vascular mechanisms subserving vasodilatation and modulation of the effects of hormones on the…
PGE2 binding sites and PG-stimulated cyclic AMP accumulation in rat isolated glomeruli and glomerular cultured cells
STIMULATION OF RENIN RELEASE BY 6‐OXO‐PROSTAGLANDIN E1 AND PROSTACYCLIN
TLDR
The prominent and sustained in vitro renin releasing effect of 6‐oxo‐PGE1, as well as the cortical localization of enzyme activity capable of generating this stable prostacyclin metabolite, suggest that formation of 6-oxo-PGE 1 may contribute to PGI2‐induced renin release and may explain the delayed stimulation caused by 6‐ oxo‐ PGF1α.
6 keto-prostaglandin-E1
Biological activities of 6-keto-prostaglandin E1.
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References

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TLDR
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TLDR
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