Monoamine oxidase and catecholamine metabolism

Kopin, Irwin J.

doi:10.1007/978-3-7091-9324-2_7

Cited by 40 publications

(39 citation statements)

References 51 publications

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“…Hypertension is also exacerbated by β1-adrenergic receptor-mediated release of renin, which will elevate arterial blood pressure by converting angiotensinogen to angiotensin I. Finally, catecholamines are inactivated and catabolized throughout the body by the enzymes catecholoxymethyltransferase and monoamine oxidase [5].…”

Section: Catecholamine Synthesis and Metabolismmentioning

confidence: 99%

Recent Insights on Circulating Catecholamines in Hypertension

Ton

Hammes

2014

Curr Hypertens Rep

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Pheochromocytomas are neuroendocrine tumors that commonly lead to excess catecholamine secretion, resulting in elevated blood pressure. In addition to potentiating vasoconstriction, catecholamines promote endothelial dysfunction, as evidenced by elevated markers of endothelial dysfunction, ADMA and sVCAM-1, in patients with pheochromcytoma. Importantly, catecholamine-induced endothelial dysfunction and hypertension may not only be due to catecholamine production by neuroendocrine tumors, as vascular endothelial cells have now been demonstrated to synthesize and secrete catecholamines. This local vascular catecholamine release appears to be triggered by hypoxia. In fact, chronic intermittent hypoxia both in vitro and in vivo leads to stabilization of hypoxic-inducible factors that increase gene expression of catecholamine-synthesizing enzymes. In an effort to target catecholamines as a means of treating hypertension, novel therapeutic options are being explored, including the generation of pharmacophores that mimic the suppressive effects of catestatin on catecholamine release as well as the use of renalase enhancers to increase catecholamine metabolism.

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Section: Catecholamine Synthesis and Metabolismmentioning

confidence: 99%

Recent Insights on Circulating Catecholamines in Hypertension

Ton

Hammes

2014

Curr Hypertens Rep

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“…Dopamine transporter and VMAT2 recycle dopamine from the extracellular space (Horn 1990; Weihe and Eiden 2000). Monoamine oxidase and COMT catabolize dopamine in the cytoplasm after reuptake by transporters (Kopin 1994; Napolitano et al 1995). Tyrosine hydroxylase and AADC are necessary for catecholamine biosynthesis (Daubner et al 2011; Molinoff and Axelrod 1971).…”

Section: Introductionmentioning

confidence: 99%

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Gaskill

Calderon

Coley

et al. 2013

J Neuroimmune Pharmacol

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Central nervous system (CNS) complications resulting from HIV infection remain a major public health problem as individuals live longer due to the success of combined antiretroviral therapy (cART). As many as 70% of HIV infected people have HIV associated neurocognitive disorders (HAND). Many HIV infected individuals abuse drugs, such as cocaine, heroin or methamphetamine, that may be important cofactors in the development of HIV CNS disease. Despite different mechanisms of action, all drugs of abuse increase extracellular dopamine in the CNS. The effects of dopamine on HIV neuropathogenesis are not well understood, and drug induced increases in CNS dopamine may be a common mechanism by which different types of drugs of abuse impact the development of HAND. Monocytes and macrophages are central to HIV infection of the CNS and to HAND. While T cells have not been shown to be a major factor in HIV-associated neuropathogenesis, studies indicate that T cells may play a larger role in the development of HAND in HIV infected drug abusers. Drug induced increases in CNS dopamine may dysregulate functions of, or increase HIV infection in, monocytes, macrophages and T cells in the brain. Thus, characterizing the effects of dopamine on these cells is important for understanding the mechanisms that mediate the development of HAND in drug abusers.

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“…[23][24][25][26] Once released, catecholamines are quickly inactivated by 2 enzymes that are responsible for their catabolism, catecholoxymethyltransferase and monoamine oxidase. 27,28 Monoamine oxidase catalyzes the oxidative deamination of amines, and catechol-oxymethyltransferase methylates the hydroxyl group meta to the side chain of catecholamines. 29 Until a few years ago, catecholamines were considered mainly as conventional neurotransmitters and neuroendocrine mediators, synthesized in the adrenal medulla.…”

mentioning

confidence: 99%

Endothelial Cells Are Able to Synthesize and Release Catecholamines Both In Vitro and In Vivo

et al. 2012

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Abstract-Recently it has been demonstrated that catecholamines are produced and used by macrophages and mediate immune response. The aim of this study is to verify whether endothelial cells (ECs), which are of myeloid origin, can produce catecholamines. We demonstrated that genes coding for tyrosine hydroxylase, Dopa decarboxylase, dopamine ␤ hydroxylase (D␤H), and phenylethanolamine-N-methyl transferase, enzymes involved in the synthesis of catecholamines, are all expressed in basal conditions in bovine aorta ECs, and their expression is enhanced in response to hypoxia. Moreover, hypoxia enhances catecholamine release. To evaluate the signal transduction pathway that regulates catecholamine synthesis in ECs, we overexpressed in bovine aorta ECs either protein kinase A (PKA) or the transcription factor cAMP response element binding, because PKA/cAMP response element binding activation induces tyrosine hydroxylase transcription and activity in response to stress. Both cAMP response element binding and PKA overexpression enhance D␤H and phenylethanolamine-N-methyl transferase gene expression and catecholamine release, whereas H89, inhibitor of PKA, exerts the opposite effect, evidencing the role of PKA/cAMP response element binding transduction pathway in the regulation of catecholamine release in bovine aorta ECs. We then evaluated by immunohistochemistry the expression of tyrosine hydroxylase, Dopa decarboxylase, D␤H, and phenylethanolamine-N-methyl transferase in femoral arteries from hindlimbs of C57Bl/6 mice 3 days after removal of the common femoral artery to induce chronic ischemia. Ischemia evokes tyrosine hydroxylase, Dopa decarboxylase, D␤H, and phenylethanolamine-N-methyl transferase expression in the endothelium. Finally, the pharmacological inhibition of catecholamine release by fusaric acid, an inhibitor of D␤H, reduces the ability of ECs to form network-like structures on Matrigel matrix. In conclusion, our study demonstrates for the first time that ECs are able to synthesize and release catecholamines in response to ischemia. Key Words: catecholamines Ⅲ ischemia Ⅲ endothelium Ⅲ angiogenesis E ndothelial cells (ECs) cover the interior surface of blood vessels throughout the entire circulatory system, and they are involved in many aspects of vascular biology.1-4 Indeed, angiogenesis is a phenomenon intimately associated with EC migration and proliferation during embryonic development. 5Similarly, ECs play major roles in immune and inflammatory reactions by regulating lymphocyte and leukocyte migration into tissues by means of direct interaction with ECs.6 Moreover, ECs have an important role in the regulation of the vascular tone by releasing vasoactive agents controlling smooth muscle cell proliferation and contractility.Indeed, ECs are known to release both vasodilators (NO) and vasoconstrictors (thromboxane, platelet-derived growth factor, and endothelin 1) in response to local and circulating stimuli. [7][8][9][10][11][12][13][14] To this purpose, the endothelium is regulated in a fine way by a s...

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Monoamine oxidase and catecholamine metabolism

Cited by 40 publications

References 51 publications

Recent Insights on Circulating Catecholamines in Hypertension

Recent Insights on Circulating Catecholamines in Hypertension

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Endothelial Cells Are Able to Synthesize and Release Catecholamines Both In Vitro and In Vivo

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