Cross-Talk between Protein Kinase A and Mitogen-Activated Protein Kinases Signalling in the Adaptive Changes Observed during Morphine Withdrawal in the Heart

Almela, Pilar; Atucha, Noemı́ M.; Milanés, M. Victoria; Laorden, María‐Luisa

doi:10.1124/jpet.109.154583

Cited by 3 publications

(4 citation statements)

References 39 publications

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“…In the heart after 90 min, there is an increase in TH protein levels, TH phosphorylation at Ser40, as well as the PKA catalytic subunit (Almela et al 2008). The increases in TH protein levels and TH phosphorylation at Ser40 are blocked by infusion of a PKA inhibitor HA-1004 (Almela et al 2008;Almela et al 2009a;Almela et al 2009b). Acute treatment of mice with haloperidol increases the phosphorylation of TH at both Ser31 and Ser40 in the striatum (Hakansson et al 2004).…”

Section: Ser40mentioning

confidence: 99%

Tyrosine hydroxylase phosphorylation in vivo

Dunkley

Dickson

2019

Journal of Neurochemistry

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Tyrosine hydroxylase (TH) is the rate‐limiting enzyme in the synthesis of the catecholamines dopamine, noradrenaline and adrenaline. One of the major mechanisms for controlling the activity of TH is protein phosphorylation. TH is phosphorylated at serine residues 8, 19, 31 and 40. There have been a number of previous reviews focused on TH phosphorylation in vitro and in situ. This review on TH phosphorylation in vivo has three main sections focusing on: (1) the methods used to investigate TH phosphorylation in vivo, including the animals used, the sacrifice procedures, the tissue preparation, the measurement of TH protein levels and TH phosphorylation and the measurement of TH activation. (2) The regulation of TH phosphorylation and its consequences in vivo, including the kinases and phosphatases acting on TH, the stoichiometry of TH phosphorylation, the proteins that bind TH and TH subcellular location. (3) The acute and prolonged TH phosphorylation changes in specific catecholaminergic tissues, including the adrenal medulla, the nigrostriatal pathway and the mesolimbic pathway.

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Section: Ser40mentioning

confidence: 99%

Tyrosine hydroxylase phosphorylation in vivo

Dunkley

Dickson

2019

Journal of Neurochemistry

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“…But chronic morphine treatment showed to decline baseline cardiovascular parameters MAP and HR. During morphine withdrawal, when naloxone was injected in morphinetreated rats, MAP and HR (26), systolic and diastolic BP were all attenuated (27). Evidences are in fader of the fact that smoking causes induced HR, SBP, DBP, and MBP (28).The increased BP following administration of nicotine may possibly be due to the induced PRA level (29).…”

Section: Discussionmentioning

confidence: 99%

Petroselinum crispum extract attenuates hepatic steatosis in rats fed with fructose enriched diet

Nair¹,

Balakrishanan²,

Santiago³

2015

BLL

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OBJECTIVE: This study was aimed to investigate the effects of addiction to nicotine and morphine and their withdrawal on coronary angiogenesis and serum NO concentrations in two-kidney one-clip hypertensive (2K1C) rats. METHODS: Male hypertensive rats were divided into the two below groups: Group (1): Rats received saline for 8 weeks (n = 8); Group (2): Rats received morphine and nicotine for 8 weeks (n = 32). At the end of 8 weeks, the groups (2) were divided into the four subgroups , which three of them were treated with withdrawal drugs. Following treatments, blood pressure, heart rate, plasma renin activity (PRA), NO concentration and capillary density were measured. RESULTS: Results showed that blood pressure was signifi cantly reduced in the addicted group when compared to non-addicted (p < 0.05). The withdrawal completely reversed blood pressure to the level observed pre-addiction (p < 0.05). Coronary angiogenesis was signifi cantly lower in the addicted group in comparistion to normal (p < 0.05) but withdrawal of addiction did not improve angiogenesis. CONCLUSION: On the basis of the present fi ndings, it may be indicative that the risk of cardiovascular complications in addiction is concurrent to chronic hypertension, which shows the importance of early diagnosis and treatment in clinical condition (Fig. 4, Ref. 59).

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“…To further investigate the role of ouabain-induced cAMP on rabbit atria, we examined the effects of ouabain and 8-Bromo-cAMP on atrial ET-1 secretion and determined that secretion was significantly increased by both agents and blocked by the PKA inhibitor H-89 and by the MAPK/ERK inhibitor PD98059. cAMP-dependent PKA signaling is related to the MAPK/ERK signaling pathway [ 7 ]. In previous work we showed that the MAPK/ERK signaling pathway is involved in the regulation of ouabain-induced atrial ET-1 secretion and to promotes atrial ANP release[ 8 ].…”

Section: Discussionmentioning

confidence: 99%

“…It is required for the activation of protein kinase A (PKA). The PKA signaling pathway is one of the most important cellular signaling pathways but it has also been shown to promote mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) phosphorylation in the heart during morphine withdrawal [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

cAMP induction by ouabain promotes endothelin-1 secretion via MAPK/ERK signaling in beating rabbit atria

Peng

Zhang

et al. 2016

Korean J Physiol Pharmacol

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Adenosine 3',5'-cyclic monophosphate (cAMP) participates in the regulation of numerous cellular functions, including the Na+-K+-ATPase (sodium pump). Ouabain, used in the treatment of several heart diseases, is known to increase cAMP levels but its effects on the atrium are not understood. The aim of the present study was to examine the effect of ouabain on the regulation of atrial cAMP production and its roles in atrial endothelin-1 (ET-1) secretion in isolated perfused beating rabbit atria. Our results showed that ouabain (3.0 µmol/L) significantly increased atrial dynamics and cAMP levels during recovery period. The ouabain-increased atrial dynamics was blocked by KB-R7943 (3.0 µmol/L), an inhibitor for reverse mode of Na+-Ca2+ exchangers (NCX), but did not by L-type Ca2+ channel blocker nifedipine (1.0 µmol/L) or protein kinase A (PKA) selective inhibitor H-89 (3.0 µmol/L). Ouabain also enhanced atrial intracellular cAMP production in response to forskolin and theophyline (100.0 µmol/L), an inhibitor of phosphodiesterase, potentiated the ouabain-induced increase in cAMP. Ouabain and 8-Bromo-cAMP (0.5 µmol/L) markedly increased atrial ET-1 secretion, which was blocked by H-89 and by PD98059 (30 µmol/L), an inhibitor of extracellular-signal-regulated kinase (ERK) without changing ouabain-induced atrial dynamics. Our results demonstrated that ouabain increases atrial cAMP levels and promotes atrial ET-1 secretion via the mitogen-activated protein kinase (MAPK)/ERK signaling pathway. These findings may explain the development of cardiac hypertrophy in response to digitalis-like compounds.

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Cross-Talk between Protein Kinase A and Mitogen-Activated Protein Kinases Signalling in the Adaptive Changes Observed during Morphine Withdrawal in the Heart

Cited by 3 publications

References 39 publications

Tyrosine hydroxylase phosphorylation in vivo

Tyrosine hydroxylase phosphorylation in vivo

Petroselinum crispum extract attenuates hepatic steatosis in rats fed with fructose enriched diet

cAMP induction by ouabain promotes endothelin-1 secretion via MAPK/ERK signaling in beating rabbit atria

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