Right atrial dilatation increases inositol‐(1,4,5)trisphosphate accumulation Implications for the control of atrial natriuretic peptide release

Harsdorf, Rüdiger von; Lang, R.; Fullerton, Meryl J.; Smith, A. Ian; Woodcock, Elizabeth A.

doi:10.1016/0014-5793(88)81384-x

Cited by 26 publications

(4 citation statements)

References 16 publications

(32 reference statements)

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“…LiCl inhibits the breakdown of Ins(1,3,4)P3 [25] {at least in the presence of Ins(1,4)P2 [26]}, but not that of Ins( 1 ,4,5)P3. The profile of release of inositol phosphates is similar to that reported previously by us in intact adult-rat heart tissue, except for the detectable peak of Ins(1,3,4)P3 at 20 min [17,27,28].…”

Section: Resultssupporting

confidence: 87%

“…This is probably a feature of the incomplete differentiation of these cells compared with the adult tissue. The pathways of inositol phosphate metabolism appear to be similar in a number of different heart preparations, isolated perfused rat heart [16,27,28], isolated guinea-pig atria [8], isolated right and left atria [7] and isolated neonatal-rat heart. This demonstrates that the absence of products of the Ins(1,4,5)P3 kinase pathway is not a feature of a particular preparation and is not related to factors such as ischaemia.…”

Section: Discussionmentioning

confidence: 99%

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Different pathways of inositol phosphate metabolism in intact neonatal rat hearts and isolated cardiomyocytes

Woodcock¹,

Tanner²,

Fullerton³

et al. 1992

Biochemical Journal

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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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Section: Resultssupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Different pathways of inositol phosphate metabolism in intact neonatal rat hearts and isolated cardiomyocytes

Woodcock¹,

Tanner²,

Fullerton³

et al. 1992

Biochemical Journal

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“…It is of interest that, in addition to preventing reperfusion arrhythmias, the aminoglycoside streptomycin has been shown to prevent arrhythmias caused by wall stress, 10 a perturbation that results in the generation of IP3. [11][12][13][14]…”

Section: Proceedings Of the Australian Physiological And Pharmacologimentioning

confidence: 99%

Inositol 1,4,5‐Trisphosphate And Reperfusion Arrhythmias

Woodcock

Arthur

Matkovich

2000

Clin Exp Pharma Physio

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1. The present review focuses on the role of the Ca2+-releasing second messenger inositol 1,4,5-trisphosphate (IP3) in initiating arrhythmias during early reperfusion following a period of myocardial ischaemia. 2. Evidence for an arrhythmogenic action of IP3 was provided by studies showing a correlation between the extent of the increase in IP3 and the incidence of arrhythmias in early reperfusion. In addition, phospholipase C inhibitors selective for thrombin receptor stimulation were anti-arrhythmic only when arrhythmias were thrombin initiated. 3. Mechanisms by which IP3 could initiate arrhythmias are discussed, with particular emphasis on the role of slow and unscheduled Ca2+ release. 4. The reperfusion-induced IP3 and arrhythmogenic responses can be initiated through either alpha1-adrenoceptors or thrombin receptors, but endothelin receptor stimulation was ineffective. Further studies have provided evidence that the noradrenaline-mediated response was mediated by alpha1A-receptors, while the alpha1B-adrenoceptor subtype appeared to be protective. 5. Reperfusion-induced IP3 responses could be inhibited by procedures known to reduce the incidence of arrhythmias under these conditions, including preconditioning, inhibiting Na+/H+ exchange or by dietary supplementation with n-3 polyunsaturated fatty acids. 6. Inositol 1,4,5-trisphosphate generation in cardiomyocytes can be facilitated by raising intracellular Ca2+ and it seems likely that the rise in Ca2+ in ischaemia and reperfusion is responsible for the generation of IP3, which will, in turn, further exacerbate Ca2+ overload.

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“…Inositol phosphates were separated using DOWEX 1 (formate) columns as described elsewhere (Woodcock et al 1987a). Analysis of the inositol mono, bis and trisphosphate fractions so obtained by anion exchange high performance liquid chromatography (HPLC) (von Harsdorf et al 1988) showed that they comprised inositol mono, bis and trisphosphate, respectively. We have previously reported the absence of products of the inositol-( 1,4,5) trisphosphate kinase pathway in rat heart (Woodcock et al 1987b;von Harsdorf et al 1989…”

Section: E T H O D Smentioning

confidence: 99%

Endothelin Stimulates Inositol Phosphate Accumulation in Rat Right and Left Atria: A Comparison With Noradrenaline

Kuraja

Woodcock

1990

Clin Exp Pharma Physio

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1. The effect of endothelin on phosphatidylinositol turnover in rat atria was investigated by measuring the generation of inositol phosphates following [3H]-inositol labelling. 2. In the presence of 10 mmol/L LiCl, endothelin caused dose-dependent increases in the accumulation of inositol mono, bis and trisphosphates which were maximal at 10(-6) mol/L endothelin. The dose-response relationship was similar in right and left atria, but right atria showed a higher maximal inositol phosphate response. 3. Endothelin produced a rapid and transient stimulation of inositol trisphosphate accumulation, which peaked at 15 s followed by a slower increase which continued linearly past 20 min. 4. The time course of inositol trisphosphate release under noradrenaline stimulation showed a similar profile but the maximum stimulation was smaller than endothelin. 5. As with endothelin, responses to noradrenaline also were higher in right atria compared with left atria. 6. These data demonstrate that endothelin receptors in rat atria are coupled to the stimulation of the phosphatidylinositol turnover pathway in an essentially similar manner to alpha 1-adrenoceptors. The phosphatidylinositol pathway may be important in mediating the reported cardiac actions of endothelin.

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Right atrial dilatation increases inositol‐(1,4,5)trisphosphate accumulation Implications for the control of atrial natriuretic peptide release

Cited by 26 publications

References 16 publications

Different pathways of inositol phosphate metabolism in intact neonatal rat hearts and isolated cardiomyocytes

Different pathways of inositol phosphate metabolism in intact neonatal rat hearts and isolated cardiomyocytes

Inositol 1,4,5‐Trisphosphate And Reperfusion Arrhythmias

Endothelin Stimulates Inositol Phosphate Accumulation in Rat Right and Left Atria: A Comparison With Noradrenaline

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