Adrenals catecholamine content

The adrenal catecholamine content of guinea pigs and rats exposed to 7.5 per cent oxygen in nitrogen for periods of 4, 8, and 12 h decreased significantly (Steinsland et al. 1970). The rate of adrenal catecholamine depletion in hypoxic rats treated with a-methyl-L-tyrosine (100 mg/k i.p.at 5-h interval) followed a patters which reflects an alteration in catecholamine release after 12 h. 

As found with guanethidine, doses of other guanidines sufficient to cause marked depletiort of noradrenaline from tissues such as heart or spleen, fail to lower the catecholamine content of the brain or adrenals. This has been shown for j3-hydroxyphenethylguanidine (LXXXVll) [265], guanisoquin (LXVII, R = 7-Br, = H) [277], 3-phenoxypropylguanidine (LXXXV) [249],... 

The major regulator of catecholamine release from the adrenal medulla is cholinergic stimulation, which causes calcium-dependent exocytosis of the contents of the secretory granules. Exocytosis of the granular content releases epinephrine (E), NE, DA, dopamine -hydroxylase, ATP, peptides, and chromaffin-specific proteins that are biologically inert. The amounts of DA and NE released are minor in comparison with that of E. Of the total catecholamine content in the granules, approximately 80% is E, 16% is NE, and the remainder is mostly DA. 

NE (levarterenol, /-noradrenahne) is released by mammalian postganglionic sympathetic nerves (Table 10-1). NE constitutes 10-20% of the catecholamine content of human adrenal medulla and as much as 97% in some pheochromocytomas, which may not express phenylethanolamine-(V-methyltransferase. 

Adrenaline is the major component of the hormonal secretion of the adrenal medulla and in the adrenal gland noradrenaline can be regarded simply as a precursor of the active substance. In sympathetic nerves, however, catecholamine synthesis proceeds no further than noradrenaline, which exists there as a transmitter substance in its own right, with properties different from those of adrenaline. Noradrenaline and small amounts of adrenaline are present in the brain also, but in addition, certain areas of the brain contain amounts of dopamine quite out of prop>ortion to their noradrenaline content and there is suggestive evidence that dopamine has an independent neurohumoral function. The unique situation thus arises that one, or probably two of the precursors of adrenaline have specialized functions of their own. 

A comprehensive investigation of the epinephrine and norepinephrine contents of adult adrenal glands was made by Lcmbeck and Obrccht (1953). On the basis of values listed for individual samples, the mean concentrations have been calculated for various age groups as st cn from Table XXVI, no significant variations with age in the total catecholamine concentration or in the proportions of epinephrine and norepinephrine were encountered between the ages of 30 and 70 years. A summary of other recent studies on adult adrenal samples is presented in Table XXVII although notable differences are noted betAveen the values observed by the various authors, no certain variation with a in the tissue catecholamine levels was reported in these publications. 

Systematic studies by Shepherd and West (1951) on the catecholamines in the adrenal glands of domestic fowl of all ages (Table XXXIII) showed much higher concentrations in this animal than in other species examined. Another remarkable finding was that norepinephrine predominates in the gland even in the adult state, and that there is little change with age in the relative norepinephrine content of the adrenal tissue. These findings have been confirmed by Akimoto and Ide (1958). 

Extractions are also sometimes necessary to remove unwanted ligands that may interfere with the binding assay. To measure the content of norepinephrine in adrenal tissue it is essential first to separate the desired ligand from the epinephrine present in this tissue, since both catecholamines will interact with the noradrenergic receptor binding sites (Enna, 1978). 

Long-term hypoxia increases TH protein content in the adrenal medulla, implying that regulation takes place at the level of gene expression (8,9) this induction, however, requires neural input to the adrenal medulla cells. There is also evidence that hypoxia may affect TH gene expression, protein synthesis, and catecholamine release in the brainstem. For example, long-term hypoxia increases TH protein content in the ventrolateral medulla, in the caudal region of the... 

The hypothalmus region was most susceptible to these changes in catecholamine biosynthesis. In spite of the observed increase in catecholamine biosynthesis in the brain and adrenals, the endogenous content of NA and DA in the brain and DA and HA in the adrenals remained unchanged . 

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