ArticleThe Biochemical journal1992
Different pathways of inositol phosphate metabolism in intact neonatal rat hearts and isolated cardiomyocytes.
Article in The Biochemical journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 36 citations in OpenAlex.
- Developmental aspects of cardiac Ca(2+) signaling: interplay between RyR- and IP(3)R-gated Ca(2+) stores.American journal of physiology. Heart and circulatory physiology · 2010Article
- Analysis of inositol phosphates in heart tissue using anion-exchange high-performance liquid chromatography.Molecular and cellular biochemistry · 1997Article
- Inositol phosphates in the heart: controversy and consensus.Journal of molecular medicine (Berlin, Germany) · 1995Review
- A low-affinity, low-molecular-mass endothelin-A receptor in neonatal rat heart.The Biochemical journal · 1994Article
- Reduction in Gh protein expression is associated with cytodifferentiation of vascular smooth muscle cells.Molecular and cellular biochemistryArticle
- Phosphoinositide-generated messengers in cardiac signal transduction.Molecular and cellular biochemistryReview
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In most tissues stimulation of the phosphatidylinositol turnover pathway causes release of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], which is subsequently metabolized to a wide range of inositol phosphate isomers deriving from both phosphorylation and dephosphorylation reactions. However, addition of noradrenaline to isolated intact neonatal-rat hearts generated only those inositol phosphates produced by dephosphorylation of Ins(1,4,5)P3. Products of the InsP3 kinase pathway were absent from the profiles, except after prolonged stimulation. In contrast, addition of noradrenaline to isolated cultured neonatal-rat cardiomyocytes caused the release of Ins(1,4,5)P3, which was metabolized by both phosphorylation and dephosphorylation pathways to yield a complex range of inositol phosphate isomers, as observed in many other cell types. These differences between the responses in intact tissues and in isolated cell preparations were not caused by the different conditions used for [3H]inositol labelling. Furthermore, results could not be explained by overgrowth of other cell types in the isolated cell preparations. Thus the results demonstrate that the isolation and culture of rat neonatal cardiomyocytes produces alterations in the nature of the phosphatidylinositol turnover pathway.
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