2004
DOI: 10.1254/jphs.fpe04001x
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Effects of Norepinephrine and Cardiotrophin-1 on Phospholipase D Activity and Incorporation of Myristic Acid Into Phosphatidylcholine in Rat Heart

Abstract: Abstract. The present study is part of a project on phospholipase D (PLD) in cardiac hypertrophy and analyzed effects on PLD activity of two growth stimuli, norepinephrine (NE) and cardiotrophin-1 (CT-1), in incubated rat heart. Phosphatidylcholine (PC) was labeled by 3 Hmyristic acid. PLD produced 3 H-phosphatidylethanol ( 3 H-PEth) from 3 H-PC in the presence of ethanol and maintained a basal formation of 3 H-PEth. Short-term and long-term exposure to NE for 2 or 13 h, respectively, enhanced the formation of… Show more

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Cited by 4 publications
(3 citation statements)
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“…7), possibly as part of a phospholipid membrane remodeling (23). The present study provided evidence, however, that the mRNA and protein expressions of PLD1 and PLD2 in the LV were markedly upregulated 30 days after banding.…”
Section: Discussioncontrasting
confidence: 61%
See 1 more Smart Citation
“…7), possibly as part of a phospholipid membrane remodeling (23). The present study provided evidence, however, that the mRNA and protein expressions of PLD1 and PLD2 in the LV were markedly upregulated 30 days after banding.…”
Section: Discussioncontrasting
confidence: 61%
“…PE was selected as agonist because α 1 -adrenoceptors play an important role in physiological and pathological cardiac hypertrophy (40,41). We did not use NE because β-adrenoceptor activation may affect PC labeling with 3 H-myristic acid (23). Chronic exposure to NE induced hypertrophic growth and gene transcription via α 1A -adrenoceptor stimulation which could be a mechanism for sustained growth (42).…”
Section: Adrenoceptorsmentioning
confidence: 99%
“…Recently, a natural phosphatidylcholine ligand for PPAR-α, 16:0/18:1-GPC, has been identified (Chakravarthy et al, 2009). As catecholamines are needed for the synthesis of some phosphatidylcholines (Weismuller et al, 2004), it is intriguing to consider that epinephrine deficiency might cause hepatic steatosis by inhibiting the formation of 16:0/18:1-GPC and thus interfere with PPAR-α function. However, after 48 h of fasting, all these regulators responded normally (and were enhanced in the case of PPAR-α and FGF-21 mRNA levels after 48 h of fasting) in epinephrine-deficient mice, indicating that their regulation is independent of epinephrine.…”
Section: Discussionmentioning
confidence: 99%