Endothelin stimulates phosphatidylinositol turnover in rat right and left atria

Kuraja, Ivana J.; Tanner, Jennifer K.; Woodcock, Elizabeth A.

doi:10.1016/0922-4106(90)90123-f

Cited by 22 publications

(13 citation statements)

References 36 publications

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“…Endothelin‐1 (ET‐1) has been demonstrated to induce inositol phosphate turnover in rat atria (15); hence, ET‐1 was used as a positive control/reference for IP 3 production in our cultured cerebral smooth muscle cells. ET‐1(10 −7 M ) rapidly increased IP 3 in cerebromicrovascular smooth muscle cells (Figs.…”

Section: Resultsmentioning

confidence: 71%

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Phospholipase C Activation by Prostacyclin Receptor Agonist in Cerebral Microvascular Smooth Muscle Cells

Parkinson

Parfenova

Leffler

2000

Proc Soc Exp Biol Med

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Abstract. The mechanism through which iloprost permits cerebral vasodilation induced by specific stimuli is incompletely understood. Previous study suggests there might be interplay between the adenylyl cyclase and phospholipase C (PLC) systems. Coupling of the prostacyclin receptor with the PLC pathway system was investigated. Iloprost, a stable prostacyclin analog, was used as a prostacyclin receptor agonist. We investigated the effects of iloprost (10−12–10−6M) on inositol 1,4,5‐trisphosphate (IP3) production by piglet cerebrovascular smooth muscle cells in primary culture. Iloprost caused concentration‐ and time‐dependent increases in IP3 production in control cells and in cells pretreated with LiCl (to prevent further IP3 metabolism). Iloprost treatment (10−12M) of cerebrovascular smooth muscle cells, in the absence and presence of 20 mM LiCl, resulted in 2‐fold and 4‐fold increases in the formation of IP3, respectively. In contrast, 10−10M to 10−6M iloprost, either in the presence or absence of LiCl, induced moderate or no increase in IP3 formation. Iloprost (10−10–10−12M) strongly stimulated diacylglycerol (DAG) generation, whereas higher concentrations (10−8M) did not induce an increase. In conclusion, the results suggest that prostacyclin receptors on cerebromicrovascular smooth muscle can couple to PLC, generating the second messengers, IP3 and DAG.

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Section: Resultsmentioning

confidence: 71%

“…5). This increase in IP 3 could be due to variation among the experiments performed, or a biphasic release of IP 3 (15). Additionally, these results do not exclude the possibility that activation of prostacyclin receptors (IP receptors) are coupled to the activation of phospholipase D and/or the breakdown of other polyphosphates.…”

Section: Discussionmentioning

confidence: 99%

Phospholipase C Activation by Prostacyclin Receptor Agonist in Cerebral Microvascular Smooth Muscle Cells

Parkinson

Parfenova

Leffler

2000

Proc Soc Exp Biol Med

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“…However, even in the presence of LiCl the 1,3,4-isomer of IP3 was only detectable in intact tissue after 20 min stimulation with noradrenaline and then at very low levels compared with the 1,4,5-isomer. It is of interest that even after 20 min stimulation with noradrenaline in the presence of LiCl no detectable peak of 1,3,4IP3 was present in intact adult heart tissue (Woodcock et al 1987;Kuraja et al 1990). Thus, while the pathway in neonatal tissue is similar to that observed in adult tissue, a small vestige of the 1,4,5IP3 kinase pathway remains.…”

Section: Discussionmentioning

confidence: 99%

“…These two arms of the pathway act in concert to initiate a wide range of physiological responses. In heart the PI turnover pathway is stimulated via a,-adrenoceptors, muscarinic cholinergic receptors and endothelin receptors (Brown et al 1985;Woodcock et al 1987;Kuraja et al 1990) and may be involved in mediating some of the responses to stimulation of these receptors.…”

Section: Introductionmentioning

confidence: 99%

Culturing Rat Neonatal Myocytes Causes Changes in the Phosphatidylinositol Turnover Pathway

Woodcock

Fullerton

Land

et al. 1991

Clin Exp Pharma Physio

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1. Cultured neonatal myocytes are commonly used as a model system for the study of cardiac phosphatidylinositol (PI) turnover. 2. In neonatal myocytes stimulation with noradrenaline causes the release of the Ca2(+)-releasing compound inositol-1,4,5-trisphosphate and the generation of the Ca2(+)-regulatory compound inositol-1,3,4,5-tetrakisphosphate. 3. Addition of noradrenaline to intact, neonatal rat hearts stimulates the release of inositol-1,4,5-trisphosphate, but not inositol-1,3,4,5-tetrakisphosphate. 4. These findings show that the isolation and culture of the neonatal myocyte causes changes in the PI turnover pathway so that it becomes similar to that described in other cell types and different from that in intact myocardial tissue. 5. The neonatal myocyte is not a useful model for the study of cardiac PI turnover.

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“…Cardiac endothelin-A (ETA) receptors, like those in other tissues, are coupled to the phosphatidylinositol (PtIns) turnover pathway and it is likely that this pathway mediates any direct cardiac actions. However, unlike ETA receptor-mediated responses in vasculature, adrenal and pituitary, ET-1 has relatively low potency at cardiac ETA receptors (Hu et al 1988b;Kuraja et al 1990), especially in the neonate (Ishikawa et al 1991). Given the low potency of ET in mediating its cardiac actions, it is unlikely to be a major effector of cardiac responses under physiological conditions, even though ET can be released locally from the coronary endothelin (Emori et al 1989).…”

Section: Introductionmentioning

confidence: 99%

A Low Affinity, Low Molecular Weight Endothelin‐a Receptor Present in Neonatal Rat Heart

Woodcock

Land

Andrews

1993

Clin Exp Pharma Physio

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1. Addition of endothelin-1 (ET-1) to [3H]-inositol-labelled neonatal rat hearts stimulated the accumulation of [3H]-labelled inositol phosphates (InsP), but only at high concentrations; concentration at half maximum stimulation (EC50) > 0.1 mumol/L). When similar experiments were performed using isolated myocytes, the potency of endothelin-1 was higher and the EC50 value averaged 3.2 +/- 0.5 nmol/L (mean +/- s.e.m., n = 4). 2. The binding affinity of [125I]-endothelin-1 was higher for receptors on isolated cells than for receptors on membranes prepared from intact heart (72 +/- 16 pmol/L compared with 3.9 +/- 0.7 nmol/L, mean +/- s.e.m., n = 4, P < 0.01; Students' t test). 3. Receptors from both sources were cross-linked to [125I]-endothelin-1 and their molecular weights measured using sodium dodecylsulfate gradient polyacrylamide gel electrophoresis (SDS-PAGE). The receptors present on the isolated cells had a higher molecular weight (48 kD) than the receptor on the heart membranes (38 kD).

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Endothelin stimulates phosphatidylinositol turnover in rat right and left atria

Cited by 22 publications

References 36 publications

Phospholipase C Activation by Prostacyclin Receptor Agonist in Cerebral Microvascular Smooth Muscle Cells

Phospholipase C Activation by Prostacyclin Receptor Agonist in Cerebral Microvascular Smooth Muscle Cells

Culturing Rat Neonatal Myocytes Causes Changes in the Phosphatidylinositol Turnover Pathway

A Low Affinity, Low Molecular Weight Endothelin‐a Receptor Present in Neonatal Rat Heart

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