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Regulation of phenylethanolamine N-methyltransferase

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    These neuroendocrine cells bear resemblance to sympathetic post-ganglionic neurons, only different in that they release their vesicular contents into the systemic circulation by way of a rich vascular network. Within the cortex of the adrenal gland, glucocorticoids released from the fasiculata layer increase the synthesis of epinephrine by increasing the half-life of PNMT mRNA and protein [23]. Both epinephrine and NE are stored in chromaffin cell vesicles and released into the circulation, although the ratio of release into the bloodstream in humans and rats is approximately 4:1, respectively [24].

  • Concentration gradient of noradrenaline from the periphery to the centre of the cornea - A clue to its origin

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    NA is the principal neurotransmitter produced and released by sympathetic nerves and these are therefore assumed to be the main reservoirs of NA in the body (Adrian et al., 1932; Smith, 1973). In some tissues (e.g. the adrenal medulla), NA is further converted to AD by the action of phenylethanolamine-N-methyltransferase and released in the systemic circulation where it is mainly responsible for sympathetic endocrine actions (Ciaranello, 1978). Active synthesis is suggested when the ratio between an enzymatic end product and its substrate is found to be higher than 1, that is, the chemical equilibrium is shifted towards the end product; the reverse is true for ratios lower than 1, which suggest a stall in production.

  • Association study of molecular polymorphisms in candidate genes related to stress responses with production and meat quality traits in pigs

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    The association between the dopamine receptor D3 DRD3(−680C>T) SNP with urinary cortisol and cortisone levels reflects the influence of this receptor on cortisol production. The change in adrenaline levels (independently from noradrenaline) may result from the influence of cortisol on adrenaline production [51] and the differences in carcass composition reflect the metabolic effects of cortisol and adrenaline (cf ante). Little is known about the regulatory effect of the dopamine receptor D3 on HPA axis and sympathetic activity.

  • Molecular genetics of the adrenocortical axis and breeding for robustness

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    We have shown, for instance, that cortisol and adrenaline levels measure in urine collected after slaughter in a genetically mixed population of pigs were highly correlated with each other, much more so than cortisol and noradrenaline levels [140,143]. One mechanism to explain this relationship is the regulation by cortisol of the enzyme PNMT, which catalyzes the methylation of noradrenaline into adrenaline [147]. It is also possible that the adrenal cortex (cortisol) and medulla (adrenaline) are somehow coactivated, but that the adrenocortical axis (cortisol) and the sympathetic nervous system (noradrenaline) are largely independent.

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