Extra-Adrenal Nonneuronal Epinephrine and Phenylethanolamine-N-Methyltransferase

Kennedy, Brian P.; Houts, Frederick W.

doi:10.1016/s1054-3589(08)60878-9

Cited by 10 publications

(7 citation statements)

References 6 publications

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“…The largest increases were seen in the left atrium and right ventricle. These data suggest that the gene expression of PNMT, which is localized mainly in heart nonneuronal cells (14,23,43), is regulated by very fast and robust processes. Cardiac PNMT activity did not follow the PNMT mRNA level increases induced by immobilization.…”

Section: Discussionmentioning

confidence: 79%

“…Cardiac ventricles contain both PNMT and NMT. Ventricular NMT can synthesize Epi from NE and also N-methyldopamine from dopamine (43).…”

Section: Discussionmentioning

confidence: 99%

“…PNMT serves as a marker for tissues and cells producing Epi. Evidence that PNMT activity is present in the heart has been reported by several authors (3,9,11,19,23,37,39,43). PNMT activity in the heart of adult rats is much lower compared with values found in newborn animals (7) or in rat fetuses (24).…”

mentioning

confidence: 81%

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Existence of cardiac PNMT mRNA in adult rats: elevation by stress in a glucocorticoid-dependent manner

Križanová

Mičutková

Jeloková

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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Phenylethanolamine N-methyltransferase (PNMT) is the enzyme that synthesizes epinephrine from norepinephrine. The aim of this study was to determine potential PNMT gene expression in the cardiac atria and ventricles of adult rats and to examine whether the gene expression of this enzyme is affected by immobilization stress. PNMT mRNA levels were detected in all four parts of the heart, with the highest level in the left atrium. Both Southern blot and sequencing verified the specificity of PNMT detected by RT-PCR. Single immobilization for 2 h increased gene expression of PNMT in both atria and ventricles. In atria, this effect was clearly modulated by glucocorticoids, because either adrenalectomy or hypophysectomy prevented the increase in PNMT mRNA levels in response to immobilization stimulus. This study establishes, for the first time, that PNMT gene expression occurs in cardiac atria and also, to a small extent, in ventricles of adult rats. Immobilization stress increases gene expression in atria and ventricles. This increase requires an intact hypothalamus-pituitary-adrenocortical axis, indicating the involvement of glucocorticoids.

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Section: Discussionmentioning

confidence: 79%

“…Cardiac ventricles contain both PNMT and NMT. Ventricular NMT can synthesize Epi from NE and also N-methyldopamine from dopamine (43).…”

Section: Discussionmentioning

confidence: 99%

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Existence of cardiac PNMT mRNA in adult rats: elevation by stress in a glucocorticoid-dependent manner

Križanová

Mičutková

Jeloková

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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“…The PNMT mRNA in the ventricles of adrenalectomized rats did not show a significant glucocorticoid influence (Krizanova et al, 2001). It is possible that ventricles of CRH knockout mice contain mainly the intron-retained PNMT mRNA form and therefore they do not respond to corticosterone deficiency during a single immobilization Ziegler et al, 1998). The phenomenon of different regulation of PNMT gene expression in the heart ventricles needs to be further studied in detail.…”

Section: Discussionmentioning

confidence: 97%

Gene Expression of Phenylethanolamine N-Methyltransferase in Corticotropin-Releasing Hormone Knockout Mice During Stress Exposure

et al. 2006

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Data show that the CRH deficiency can markedly prevent immobilization-triggered induction of the PNMT mRNA and protein levels in the adrenal medulla and stellate ganglia. Reduced plasma epinephrine and corticosterone levels and adrenal medullary EGR-1 protein levels in CRH knockout versus WT mice during stress indicate that the HPA axis plays a crucial role in regulation of the PNMT gene expression in these organs. Cardiac atrial PNMT gene expression with stress is also dependent on intact HPA axis. However, in cardiac ventricles, especially after the single stress exposure, its expression is not impaired by CRH deficiency. Since cardiac EGR-1 protein levels in CRH KO mice are also not affected by the single stress exposure, we propose existence of different regulation of the PNMT gene expression, especially in the cardiac ventricles.Overall, our findings reveal that the PNMT gene expression is regulated through the HPA in both sympathoadrenal system and the heart and also via EGR-1 in the adrenal medulla, but apparently not in the heart. Regulation of the PNMT gene expression in various compartments of heart includes both corticosterone-dependent and independent mechanisms.

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“…When an adrenalectomized rat received intravenous 3 H‐methionine into its renal arteries, 3 H‐epinephrine appeared in the urine 11. Radiotracer studies also indicate that a large fraction of human urinary epinephrine is made renally 12. Preliminary estimates indicate that 43% of urine epinephrine is made in the human kidney and that this fraction may be appreciably higher in hypertensive humans.…”

Section: Locationmentioning

confidence: 99%

Location, Development, Control, and Function of Extraadrenal Phenylethanolamine N‐Methyltransferase

Ziegler

Bao

Kennedy

et al. 2002

Annals of the New York Academy of Sciences

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Phenylethanolamine N-methyltransferase (PNMT) methylates norepinephrine (NE) to form epinephrine (E). It is present in a high concentration in the adrenal medula but occurs in many other tissues throughout the body. In the brain stem and retina PNMT is present in specific neurons. Cardiac PNMT develops early in the fetal heart and is found in relatively high levels in the adult left atrium. Intrinsic cardiac adrenergic cells are distributed throughout the adult myocardium and contain all the enzymes necessary for E synthesis. The PNMT gene promoter region contains a glucocorticoid response element; however, the initial development of brain and cardiac fetal PNMT is glucocorticoid independent. Rat fetal heart PNMT peaks at embryonic day 11 and becomes sensitive to glucocorticoid induction by day 12. PNMT-containing cells are concentrated in the atrioventricular canal and interventricular septum during cardiac development, areas important in the development of the cardiac conduction system. In the adult rat, cardiac PNMT is inducible by glucocorticoids and synthesizes E. Glucocorticoids are essential for development of the high levels of PNMT in the adrenal, but are less important outside the adrenal. The PNMT gene contains 3 exons and 2 introns. Adrenal PNMT mRNA exists as a single type, but in the heart PNMT mRNA is present as both an intronless and an intron-containing type. In some cardiac tissues, glucocorticoids decrease levels of intron-containing PNMT mRNA and increase intronless PNMT mRNA and PNMT activity. Studies in adrenalectomized animals suggest that extraadrenal PNMT increases blood pressure, blood glucose, and lymphocyte cytokine production. PNMT may also play a role in the regulation of fetal heart rate prior to development of the adrenal medulla.

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Extra-Adrenal Nonneuronal Epinephrine and Phenylethanolamine-N-Methyltransferase

Cited by 10 publications

References 6 publications

Existence of cardiac PNMT mRNA in adult rats: elevation by stress in a glucocorticoid-dependent manner

Existence of cardiac PNMT mRNA in adult rats: elevation by stress in a glucocorticoid-dependent manner

Gene Expression of Phenylethanolamine N-Methyltransferase in Corticotropin-Releasing Hormone Knockout Mice During Stress Exposure

Location, Development, Control, and Function of Extraadrenal Phenylethanolamine N‐Methyltransferase

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