Serum dopamine-beta-hydroxylase activity: sibling-sibling correlation

Dopamine-beta-hydroxylase activity is released into the blood with catecholamines from the adrenal medulla and sympathetic nerves. This enzyme activity has been measured in the blood of 317 normal children and 227 normal adults. A significant sibling-sibling correlation of serum dopamine-beta-hydroxylase values was found in the 94 sibling pairs tested. Frequency distributions of serum enzyme values in both children and adults suggest the existence of two populations with regard to serum activity of this enzyme.     

Quantal secretion from adrenal medulla: all-or-none release of storage vesicle content

Neurogenic secretion of catecholamines from the adrenal medulla in rabbits, induced by administration of insulin, caused decreases in both the dopamine-beta-hydroxylase activity and the catecholamine content of the storage vesicle fraction. After sedimentation through a sucrose density gradient, the storage vesicles obtained from insulin-treated animals had the same density and the same ratio of dopamine-beta-hydroxylase to catecholamine as did vesicles from untreated animals. These and other data indicate that neurogenic secretion from the adrenal medulla occurs by an all-or-none release from the storage vesicles.     

Adrenaline synthesis: control by the pituitary gland and adrenal glucocorticoids

The activity of phenylethanolamine-N-methyl transferase, an enzyme that synthesizes adrenaline from noradrenaline in the adrenal medulla, is markedly depressed following hypophysectomy. Enzyme activity is restored to normal after administration of ACTH or the potent glucocorticoid, dexamethasone. Thus the biosynthesis of adrenaline in the adrenal medulla appears to be regulated by the pituitary-adrenocortical system.     

Delta 9 -tetrahydrocannabinol and ethanol: differential effects on sympathetic activity in differing environmental setting

Serum dopamine beta-hydroxylase activity, a useful biochemical index of peripheral sympathetic nervous activity, was measured in rats treated with Delta(9)-tetrahydrocannabinol or ethanol or both substances. After 7 days of treatment with either substance, serum dopamine beta-hydroxylase activity decreased significantly. Combined treatment with both agents enhanced the effects of each given alone. In rats subjected to immobilization stress, treatment with Delta(9)- tetrahydrocannabinol appeared to potentiate the stress-induced increase in serum enzyme activity. Treatment with ethanol, with or without Delta(9)-tetrahydrocannabinol, effectively blocked this increase in enzyme activity. These results show that both substances have significant effects on the sympathetic nervous system which are critically influenced by environmental setting.     

Involvement of adenosine 3',5'-monophosphate in the activation of tyrosine hydroxylase elicited by drugs

Immediately after the injection of reserpine (16 micromoles per kilogram, intraperitoneally), aminophylline (200 micromoles per kilogram, intraperitoneally), and carbamylcholine (8.2 micromoles per kilogram, intraperitoneally), the concentration of adenosine 3',5'-monophosphate in adrenal medulla of rats is increased severalfold. The three drugs also cause a delayed increase of medullary tyrosine hydroxylase activity. Our results are consistent with the view that an increase of medullary adenosine 3',5'-monophosphate concentration is involved in the drug-induced increase of tyrosine hydroxylase activity in adrenal medulla. Experiments with tyramine (130 micromoles per kilogram, intraperitoneally) suggest that the increase of tyrosine hydroxylase activity and of adenosine 3',5'-monophosphate concentrations is independent of an increase in adrenal catecholamine turnover rate.     

Pineal N-acetyltransferase activity: effect of sympathetic stimulation

Stimulation of preganglionic sympathetic fibers to the superior cervical ganglia elevates the activity of pineal N-acetyltransferase. After the stimulation-induced rise in enzyme activity, a return toward baseline levels occurs whether or not nerve stimulation is continued. The ability of pineal N-acetyltransferase activity to fall in the presence of stimulation may account for the persistence of its rhythm in blinded animals.     

Adrenal tyrosine hydroxylase: compensatory increase in activity after chemical sympathectomy

Destruction of peripheral sympathetic nerve endings with 6-hydroxydopamine causes a disappearance of cardiac tyrosine hydroxylase, accompanied by a twofold increase in adrenal tyrosine hydroxylase and a small increase in phenyl-ethanolanine-N-methyl transferase. No change in adrenal catecholamine content occurs under these conditions.     

中国水牛肾上腺光镜和电镜观察

对成年的湖南滨湖水牛肾上腺光镜和电镜观察结果表明，肾上腺外面被覆一层较厚的被膜，内分皮质部和髓质部．四周为皮质部，呈深黄色，约占肾上腺７０％，中央为髓质部，呈灰白色，约占肾上腺３０％．Ｈ－Ｅ染色法将皮质部分为３个小区，即球状区，束状区和网状区．球状区薄，细胞染色较深；束状区厚，胞质呈蜂窝状，细胞染色浅；网状区细胞与髓质交界参差不齐，胞核呈退化变性现象，染色较深．髓质部比皮质部染色浅，常分为外区和内区．外区细胞大，呈高柱状，主要由肾上腺素细胞组成；内区细胞较小，呈立方或多边形，由去甲肾上腺素细胞和肾上腺素细胞组成，去甲肾上腺素细胞分散于肾上腺素细胞之间．髓质部还有少数分散的大型交感神经节细胞，且内区比外区多．     

Acetylcholinesterase regeneration in peripheral nerve after irreversible inactivation

The return of acetylcholinesterase activity was studied in several cholinergic structures in the cat after irreversible inactivation by diisopropylfluoro-phosphate. It was found that enzymic activity returned uniformly along the hypoglossal and cervical sympathetic nerve trunks. No evidence for somatoaxonal convection of enzyme was obtained.     

Septal tryptophan-5-hydroxylase: divergent response to raphe lesions and parachlorophenylalanine

A soluble form of tryptophan-5-hydroxylase activity was found to be present in areas rich in serotonergic terminals (colliculi, hippocampus, septal area, and remaining telencephalon) as well as in brainstem, an area rich in cell bodies. The enzymatic activity in all brain regions, except the septal area, was inhibited to varying degrees following administration of parachlorophenylalanine. Destruction of the raphe nuclei in the midbrain led to a large and comparable decrease in both serotonin content and tryptophan hydroxylase activity of the hippocampus. In contrast, these lesions did not significantly affect the enzymatic activity of the septal area although the serotonin content was decreased by 72 percent. These findings suggest that the major portion of the tryptophan hydroxylase activity of the septal area is uniquely different from that found in other telencephalic areas in that it is not localized in serotonergic nerve terminals nor is it inhibited by parachlorophenylalanine.     

Dopamine-beta-hydroxylase: evidence for increased activity in sympathetic neurons during psychotic states

Tritiated dopamine was infused into psychiatric patients during acute psychotic episodes and in remission. An index of the activity of dopamine-beta-hydroxylase of salivary gland sympathetic neurons was determined by measuring the distribution of tritiated metabolites in salivary fluid. Increased synthesis of norepinephrine occurred in acute schizophrenia and in the manic state of manic-depressive psychosis but not in the depressed phase.     

鸡腔上囊传出神经元的分布——用CB—HRP法研究

将CB—HRP注入鸡腔上囊壁内,支配腔上囊的神经元被标记。支配腔上囊的长轴突型交感节前神经元在胸7—腰荐3(简称T_7—LS_3)髓节的Terni氏柱内,主要位于LS_1—LS_2髓节。在LS_8—LS_(11)髓节中央管背侧和背外侧区有大量标记细胞,主要集中于LS_8髓节,这些标记细胞是支配腔上囊的副交感节前神经元,其轴突大部分行经同侧盆神经到达腔上囊,少数行经对侧的盆神经到达腔上囊。腔上囊的交感节后神经元位于T_6—L_(13)交感干神经节和肾上腺神经节,交感干的标记细胞集中位于LS_9—LS_(11)和LS_2—LS_3。副交感节后神经元位于盆神经和泄殖腔神经节内。在肠神经内有大量的标记细胞。     

Renal concentrating mechanism: possible role for sodium-potassium activated adenosine triphosphatase

Sodium-potassium activated adenosine triphosphatase activity was found to be almost twice as high in renal medulla as in cortex. Infusion of digoxin, a specific inhibitor of the enzyme, into one renal artery of the dog resulted in unilateral natriuresis, impaired concentrating capacity, and reduction of the enzyme activity in both cortex and medulla. It is suggested that the sodium-potassium adenosine triphosphatase plays an important role in urine concentration mechanisms.     

The dorsal aorta initiates a molecular cascade that instructs sympatho-adrenal specification

The autonomic nervous system, which includes the sympathetic neurons and adrenal medulla, originates from the neural crest. Combining avian blood vessel-specific gene manipulation and mouse genetics, we addressed a long-standing question of how neural crest cells (NCCs) generate sympathetic and medullary lineages during embryogenesis. We found that the dorsal aorta acts as a morphogenetic signaling center that coordinates NCC migration and cell lineage segregation. Bone morphogenetic proteins (BMPs) produced by the dorsal aorta are critical for the production of the chemokine stromal cell-derived factor-1 (SDF -1) and Neuregulin 1 in the para-aortic region, which act as chemoattractants for early migration. Later, BMP signaling is directly involved in the sympatho-medullary segregation. This study provides insights into the complex developmental signaling cascade that instructs one of the earliest events of neurovascular interactions guiding embryonic development.     

Adrenergic excitation of cutaneous pain receptors induced by peripheral nerve injury

The mechanisms by which peripheral nerve injuries sometimes lead to causalgia, aberrant burning pain peripheral to the site of nerve damage, are uncertain, although the sympathetic nervous system is known to be involved. Whether such syndromes could be the result of the development of responsiveness by some cutaneous pain receptors (C-fiber nociceptors) to sympathetic efferent activity as a consequence of the nerve injury was tested in an animal model. After nerve damage but not in its absence, sympathetic stimulation and norepinephrine were excitatory for a subset of skin C-fiber nociceptors and enhanced the responsiveness of these nociceptors to tissue-damaging stimulation. These effects were demonstratable within days after nerve lesions, occurred at the cutaneous receptive terminal region, were manifest in sensory fibers that had not degenerated after the injury, and were mediated by alpha 2-adrenergic-like receptors.     

Narcotic drugs: effects on the serotonin biosynthetic systems of the brain

The effects of short- and long-term administration of morphine on the activity of two measurable forms of rat brain tryptophan hydroxylase were studied. Morphine administration produced an immediate decrease and a longterm increase in the nerve ending (particulate) enzyme activity but did not change the cell body (soluble) enzyme activity. Cocaine administration demnonstrated a short-term decrcease in measurable nerve eniding enzyme activity that was due to the inhibition of the high affinity uptake (the Michaelis constant, K(m) is 10-(5) molar) of trytophan, the serotonin precursor. Cocaine did not aflect the low affinity uptake K(m) = 10-(5) molar) of tryptophan. Both the uptake of the precursor and the enizymiie activity appeared to be drug-sensitive regullatory processes in the biosynthlesis of serotonin.     

Rat fighting behavior: serum dopamine- -hydroxylase and hypothalamic tyrosine hydroxylase

Male Sprague-Dawley rats were subjected to 4 weeks of daily periods of immobilization stress. One of two experimental groups was allowed 1 month of recovery. After 4 weeks of stress, there was a significant increase in shockinduced fighting, in the activity of serum dopamine-beta-hydroxylase, and in the activity of hypothalamic tyrosine hydroxylase. The concentration of hypothalamic norepinephrine was not decreased. After 4 weeks of recovery, only serum dopamine-betahydroxylase activity returned to normal; it therefore appears that longterm stress may increase central catecholamine synthesis. possibly resulting in a persistent increase in aggressive behavior.     

Identification of pro-opiomelanocortin-derived peptides in the human adrenal medulla

Extracts from adult human adrenals contained high concentrations of immunoreactive beta-endorphin and alpha-melanotropin. Lower quantities of immunoreactive adrenocorticotropic hormone could also be detected. Distribution studies showed the presence of pro-opiomelanocortin fragments in the adrenal medulla. No alpha-melanotropin, beta-endorphin, or adrenocorticotropic hormone could be found in adrenal extracts from several other mammalian species. Analysis of the beta-endorphin-like immunoreactivity using region specific radioimmunoassays interfacing with gel filtration and reverse-phase high-performance liquid chromatography showed the majority of the beta-endorphin-like material to exist as nonacetylated beta-endorphin-(1-31) with a small percentage of lipotropin-sized molecules. The alpha-melanotropin-like immunoreactivity cochromatographed on gel filtration and reverse-phase high-performance liquid chromatography with desacetyl alpha-melanotropin. The data suggest that pro-opiomelanocortin is expressed in the adrenal medulla of humans but is not detectable in the adrenal glands of many other mammalian species.     

Axonal transport of dopamine- -hydroxylase by human sural nerves in vitro

Dopamine-beta-hydroxylase activity accumulated above a ligature on biopsy samples of normal human sural nerves incubated in vitro. The rate of accumulation indicated that this enzyme was transported distally at a velocity of 2 millimeters per hour. Axoplasmic transport of dopamine-beta-hydroxylase was greatly reduced in sural nerves from a few patients with peripheral neuropathies.     

Neurogenic Component of Chronic Renal Hypertension

Infusion of angiotensin or renin in small quantities affects the sympathetic nervous system so that responses are increased to either drugs or reflexes that cause release of norepinephrine at nerve endings. Response to injected norepinephrine is relatively unchanged. This action of angiotensin is dependent upon an intact sympathetic nervous system. The direct vasoconstrictor action of angiotensin is not an essential part of the enhanced response. The phenomenon was shown to have relevance to acute and chronic experimental renal hypertension in dogs by the fact that in both the pressor response to tyramine was enhanced. We believe that the ability of angiotensin to intensify the effect of normal neurogenic vasomotor activity, along with an upward reset of the carotid sinus buffer mechanism, might account importantly for the neurogenic component of renal hypertension.