Incubation of cultured bovine adrenal medullary cells with p-chloromercuribenzoate (50-500 microM), a sulfhydryl-reacting agent, caused an increase in the secretion of catecholamines, p-Chloromercuriphenyl sulfonate, a p-chloromercuribenzoate analogue that poorly penetrates the cell membrane, caused a similar increase in catecholamine secretion. In both cases, catecholamine secretion was dependent on extracellular Ca2+. Furthermore, p-chloromercuribenzoate caused both 45Ca2+ influx into the cells and an increase in the intracellular free Ca2+ concentration. The increases in catecholamine secretion and 45Ca2+ influx behaved similarly in relation to p-chloromercuribenzoate concentration. The time courses of the increased secretion, 45Ca2+ influx, and intracellular free Ca2+ concentration by p-chloromercuribenzoate were also quite similar. The stimulation of catecholamine secretion by p-chloromercuribenzoate was reversed by washing the cells with dithiothreitol-containing medium, but not by dithiothreitol
Cultures of bovine adrenomedullary chromaffin cells accumulated 1-methyl-4-phenylpyridinium (MPP+) in a time- and concentration-dependent manner by a process that was prevented by desmethylimipramine. The subcellular localization of the incorporated [methyl-3H]MPP+ was examined by differential centrifugation and sucrose density gradient fractionation and was found to be predominantly colocalized with catecholamines in chromaffin vesicles, and negligible amounts were detected within the mitochondrial fraction. When chromaffin cell membranes were made permeable with the detergent digitonin in the absence of calcium, there was no increase in the release of [3H]MPP+, indicating that there is negligible accumulation of the neurotoxin in the cytosol. Simultaneous exposure to digitonin and calcium induced cosecretion of MPP+ and catecholamines. Stimulation of the cells with nicotine released both catecholamines and MPP+ at identical rates and percentages of cellular content in a calcium-dependent ...
Neonatal sympathectomy using a combined treatment with antiserum to nerve growth factor and guanethidine during the first 4 weeks after birth was carried out in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Bilateral adrenal demedullation was performed in 4-week-old sympathectomized SHR and WKY rats. The development of hypertension in SHR was prevented by sympathectomy, but the blood pressure (BP) was still higher than in age-matched WKY rats. Demedullation reduced the BP of sympathectomized SHR to the same level as that of WKY rats. Heart rates of SHR and WKY rats were not affected by the treatments. Morphometric measurements of the mesenteric arteries showed that sympathectomy significantly reduced the medial mass in the mesenteric arteries of SHR, mainly through a reduction in the number of smooth muscle cell layers. In sympathectomized SHR, demedullation increased the lumen size of muscular arteries under maximally relaxed conditions, which might explain the ...
Catecholamine secretion in the bovine adrenal medulla is evoked largely by nicotinic receptor activation. However, bovine adrenal medulla also contain muscarini
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We have demonstrated previously that spontaneously diabetic BB-Wistar rats exhibit decreased adrenal medullary catecholamine secretion in response to splanchnic nerve terminal stimulation. We hypothesized that this abnormality is caused by changes in the sensitivity of the adrenomedullary chromaffin cells to acetylcholine (ACh). To study this hypothesis, we isolated adrenal glands from control and spontaneously diabetic BB-Wistar rats, perfused them with ACh, and measured catecholamine secretion. Adrenal catecholamine release in response to ACh was significantly decreased at 2, 8, and 16 weeks after the onset of diabetes compared with age-matched, nondiabetic control rats. Catecholamine release in response to perfusion with 20 mM K+ was the same in adrenals from diabetic and control rats. The decreased responsiveness of diabetic rat adrenals to perfusion with ACh was significantly correlated with a decrease in the release of catecholamines in response to splanchnic nerve stimulation. A similar ...
Rat pheochromocytoma cells (PC 12) permeabilized with staphylococcal α-toxin release [3H]dopamine after addition of micromolar Ca2+. This does not require additional Mg2+-ATP (in contrast to bovine adrenal medullary chromaffin cells). We also observed Ca2+-dependent [3H]-dopamine release from digitonin-permeabilized PC 12 cells. Permeabilization with α-toxin or digitonin and stimulation of the cells were done consecutively to wash out endogenous Mg2+-ATP. During permeabilization, ATP was removed effectively from the cytoplasm by both agents but the cells released [3H]dopamine in response to micromolar Ca2+ alone. Replacement by chloride of glutamate, which could sustain mitochondrial ATP production in permeabilized cells, does not significantly alter catecholamine release induced by Ca2+. However, Mg2+ without ATP augments the Ca2+-induced release. The release was unaltered by thiol-, hydroxyl-, or calmodulin-interfering substances. Thus Mg2+-ATP, calmodulin, or proteins containing -SH or -OH ...
Synonyms for adrenomedullary hormones in Free Thesaurus. Antonyms for adrenomedullary hormones. 2 synonyms for hormone: endocrine, internal secretion. What are synonyms for adrenomedullary hormones?
Looking for adrenomedullary hormone? Find out information about adrenomedullary hormone. secretory substance carried from one gland or organ of the body via the bloodstream to more or less specific tissues, where it exerts some influence upon... Explanation of adrenomedullary hormone
1. The lipid composition of the membranes from isolated 5-hydroxytryptamine-storage organelles of blood platelets of rabbits and of those from chromaffin granules of bovine adrenal medulla was compared. 2. In contrast with the membranes of the chromaffin granules, those of the 5-hydroxytryptamine organelles did not contain lysophosphatidylcholine (lysolecithin). 3. Both the cholesterol/phospholipid ratio and the relative proportions of phosphatidylethanolamine (kephalin), phosphatidylinositol and phosphatidylserine were about the same in both membranes, whereas phosphatidylcholine (lecithin) and sphingomyelin showed somewhat higher values in the membranes of the 5-hydroxytryptamine organelles. 4. In conclusion, the release of 5-hydroxytryptamine from blood platelets is probably not correlated with the presence of lysophosphatidylcholine in the membranes of the storage organelles and may thus differ from the mechanism of catecholamine release in adrenal medulla.. ...
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Area of interest: Mechanisms of stress transduction at the sympatho-adrenal synapse; optical studies of hormone trafficking and secretion in the adrenomedullary chromaffin cell.
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OK, so say a llama charges you, do you flee or do you fight? This instantaneous response is mediated by a group of hormones called catecholamines. The two main catecholamines responsible for the fight-or-flight response are norepinephrine and epinephrine (also called noradrenaline and adrenaline). When your brain perceives something as dangerous, it activates your sympathetic nervous system (SNS). The SNS activates preganglionic sympathetic nerves that innervate the adrenal medulla (the adrenal medulla is the inner part of the adrenal gland, you have two adrenal glands that sit on top of each of your kidneys). These nerves form synapses with cells that produce norepinephrine and epinephrine (these are called chromaffin cells, each individual cell can produce only norepinephrine or epinephrine, never both). Activated preganglionic sympathetic nerves release acetylcholine into the synapse, which causes chromaffin cells to increase their membrane conductance for Ca2+, which then causes ...
OK, so say a llama charges you, do you flee or do you fight? This instantaneous response is mediated by a group of hormones called catecholamines. The two main catecholamines responsible for the fight-or-flight response are norepinephrine and epinephrine (also called noradrenaline and adrenaline). When your brain perceives something as dangerous, it activates your sympathetic nervous system (SNS). The SNS activates preganglionic sympathetic nerves that innervate the adrenal medulla (the adrenal medulla is the inner part of the adrenal gland, you have two adrenal glands that sit on top of each of your kidneys). These nerves form synapses with cells that produce norepinephrine and epinephrine (these are called chromaffin cells, each individual cell can produce only norepinephrine or epinephrine, never both). Activated preganglionic sympathetic nerves release acetylcholine into the synapse, which causes chromaffin cells to increase their membrane conductance for Ca2+, which then causes ...
First cultured by Greene and Tischler in 1976, PC-12 cells originated from a pheochromocytoma (neuroendocrine tumor) of the rat adrenal medulla. It was developed as a model cell line and an alternative to adrenal chromaffin primary cell cultures. PC-12 cells are able to differentiate into neuron-like cells in the presence of nerve growth factor or dexamethasone. Due to their differentiation ability and ease of culture, PC-12 cells are used in a variety of research areas ranging from drug efficacy to neurosecretion.. ...
The role of nongenomic action of estrogens on elicited catecholamine secretion and exocytosis kinetics was studied in perfused rat adrenals and in cultured bovine chromaffin cells. 17β-Estradiol as well as the estrogen receptor modulators raloxifene and LY117018, but not 17α-estradiol, inhibited at the micromolar range the catecholamine output elicited by acetylcholine or high potassium. However, these agents failed to modify the secretion elicited by high Ca2+ in glands treated with the ionophore A-23187 (calcimycin), suggesting that estrogens did not directly act on the secretory machinery. At the single cell level, estrogens modified the kinetics of exocytosis at nanomolar range. All of the drugs tested except 17α-estradiol produced a profound slowing down of the exocytosis as measured by amperometry. LY117018 also reduced the granule content of catecholamines. 17β-Estradiol reduced the intracellular free Ca2+ but only at micromolar concentrations, whereas nanomolar concentrations ...
The adrenal gland is a paired retroperitoneal organ located on the upper pole of each kidney. It receives its arterial supply from the superior, middle, and in…
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the case.. a 44 year old male presents to your Emergency Department with severe, crushing retrosternal chest pain. He reports that the pain started suddenly approximately one hour ago whilst at rest.. [Read more…]. ...
Mice, Peroxisome, Role, Knockout Mice, Liver, Peroxisomes, Adipose Tissue, Adrenal Medulla, Nervous System, Neurons, Peripheral Nervous System, Tissue, Tissues, Biogenesis, Pathologies, Patients, Cell, Hepatocytes, Organelles, Metabolism
In bovine adrenal chromaffin cells, prostaglandin E2 (PGE2) stimulates the formation of inositol phosphates and Ca2+ mobilization through its specific receptor [Yokohama, Tanaka, Ito, Negishi, Hayashi & Hayaishi (1988) J. Biol. Chem. 263, 1119-1122]. Here we show that PGE2-induced phosphoinositide metabolism was blocked by pretreatment with 12-O-tetradecanoylphorbol 13-acetate (TPA). Using intact cells, we also examined the inhibitory effect of TPA on the individual steps of the activation process of phosphoinositide metabolism. The inhibition was observed within 1 min and complete by 10 min after addition of 1 microM-TPA, and half-maximal inhibition by TPA occurred at 20 nM. TPA prevented Ca2+ mobilization induced by PGE2, but not by the Ca2+ ionophore ionomycin. The inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate did not inhibit the formation of inositol phosphates and Ca2+ mobilization by PGE2. TPA treatment affected neither the high-affinity binding of [3H]PGE2 to intact cells and ...
Explants of rat adrenal medulla were grown in tissue culture. The effects of various doses of dbcAMP ranging from 0.001 mM up to 1 mM and equimolar amounts of theophylline were recorded by phase contrast optics and catecholamine histochemistry (glyoxylic acid method) over six days. There was a dose-dependent inhibition of the normally occurring outgrowth of Schwann cells, chromaffin cells and axons from the explants. Maintenance of glyoxylic acid-induced fluorescence in chromaffin cells was dose-dependent, too. Since theophylline is known to enhance intracellular levels of cAMP only, these effects are probably due to the action of cAMP. cAMP obviously maintains the degree of differentiation of chromaffin cells. Thus it could be argued that a certain degree of dedifferentiation is a prerequisite for the formation of axons from these cells. ...
The ACh-stimulated increase in [Ca2+]i in bovine adrenal chromaffin cells is mainly triggered by an influx of Ca2+ through the nAChR channel, VOC, and the subsequent activation of Ca2+-induced Ca2+ release, all of which contribute to CA release. These events in response to ACh are of short duration, whereas PACAP induces large and sustained increases in [Ca2+]i and CA release. The present study sought to elucidate which pathways (nAChR channel, VOC, SOC, or an unidentified channel) contribute to this peculiar Ca2+ and secretory response to PACAP.. Reports vary concerning the effect of VOC blockers on PACAP-induced rise in [Ca2+]i and CA release. For example, Przywara et al. (1996) showed that in rat cultured adrenal chromaffin cells, neither L- nor N-type VOC participates in the PACAP-induced CA release. On the other hand,Fukushima et al. (2001b) showed that nifedipine, L-type VOC antagonist, reduced PACAP-induced CA release in isolated perfused rat adrenal gland. Tanaka et al. (1996) reported ...
Marley, PD, McLeod, J, Anderson, C and Thompson, KA 1995, Nerves containing nitric oxide synthase and their possible function in the control of catecholamine secretion in the bovine adrenal medulla, Journal of the Autonomic Nervous System, vol. 54, no. 3, pp. 184-194, doi: 10.1016/0165-1838(95)00013-N. ...
Adrenomedullary chromaffin cells have been used as an excellent experimental model to study the exocytosis and therefore the molecular mechanisms of neurotransmission. It is now clear that the proteins involved in the processes of vesicle docking, membrane fusion and neurotransmitter release are common to many cellular systems (SNARE hypothesis). Our research interest is focused in two different aspects of the molecular mechanisms of neurotransmission: Implication of molecular motors such myosin-actin in vesicle transport during neurosecretion and the determination of essential aminoacids of synaptobrevin or SNAP-25 implicated in the process of membrane fusion. Experimental approaches involve strategies using antibodies, sequence peptide design and protein overexpression that demonstrate the participation of specific protein domains in exocytosis. In addition, the role of these proteins on the secretory stages have been studied using amperometry, technique that resolves single fusion events ...
Adrenomedullary chromaffin cells have been used as an excellent experimental model to study the exocytosis and therefore the molecular mechanisms of neurotransmission. It is now clear that the proteins involved in the processes of vesicle docking, membrane fusion and neurotransmitter release are common to many cellular systems (SNARE hypothesis). Our research interest is focused in two different aspects of the molecular mechanisms of neurotransmission: Implication of molecular motors such myosin-actin in vesicle transport during neurosecretion and the determination of essential aminoacids of synaptobrevin or SNAP-25 implicated in the process of membrane fusion. We coined the term "Molecular cytoarchitecture of exocytosis" to define the interaction between SNARE proteins, calcium channel and lately nicotinic receptors (integrating Dr. Criado main line) and the cohesive F-actin cortical network in order to improve secretory efficiency ...
As its name suggests, the adrenal medulla is the central core of the adrenal gland, surrounded by the adrenal cortex. The chromaffin cells of the medulla are the bodys main source of the catecholamine hormones adrenaline (epinephrine) and noradrenaline (norepinephrine). These water-soluble hormones, derived from the amino acid tyrosine, are part of the fight-or-flight response initiated by the sympathetic nervous system. The adrenal medulla can be considered specialized ganglia of the sympathetic nervous system, lacking distinct synapses, instead releasing secretions directly into the blood. It is also the main source of dopamine, a catecholamine closely related to adrenaline and noradrenaline ...
As its name suggests, the adrenal medulla is the central core of the adrenal gland, surrounded by the adrenal cortex. The chromaffin cells of the medulla are the bodys main source of the catecholamine hormones adrenaline (epinephrine) and noradrenaline (norepinephrine). These water-soluble hormones, derived from the amino acid tyrosine, are part of the fight-or-flight response initiated by the sympathetic nervous system. The adrenal medulla can be considered specialized ganglia of the sympathetic nervous system, lacking distinct synapses, instead releasing secretions directly into the blood. It is also the main source of dopamine, a catecholamine closely related to adrenaline and noradrenaline ...
Our previous study demonstrated that microinjection of leptin into the ventromedial hypothalamus (VMH) dramatically increased glucose uptake in the heart, brown adipose tissue (BAT), and skeletal muscles, but not in white adipose tissue (WAT) in conscious unrestrained rats, as assessed in vivo by the 2-[3H]deoxyglucose method. Here we examined the role of the sympathetic nervous system and insulin in enhanced glucose uptake by tissues after hypothalamic leptin injection. Pretreatment with guanethidine significantly suppressed the increased glucose uptake by the tissues in response to leptin injected into the VMH, whereas bilateral adrenal demedullation had no significant effect. Treatment with propranolol but not phenoxybenzamine also decreased significantly enhanced glucose uptake by the tissues. We further examined the interaction of the effects of hypothalamic leptin and insulin administered peripherally by clamping the glucose concentrations at a constant level. When leptin was injected into ...
Passage of current for brief periods through electrodes in the lateral hypothalamus virtually always resulted in a distinctive biphasic hyperglycaemia in the case of electrodes capable of eliciting feeding at similar current intensities. The biphasic hyperglycaemic response was sometimes elicited by electrodes aimed at the feeding area but not capable of eliciting feeding. The response remained under pentobarbital anaesthesia. Electrodes in other regions of the hypothalamus gave monophasic hyperglycaemia or hypoglycaemia or no blood glucose change. The hyperglycaemic phases of the biphasic response were diminished by an adrenergic alpha-receptor blocking agent and by bilateral adrenal demedullation. The intermediate lowering of blood glucose concentration could be eliminated by injection of atropine or by sub-diaphragmatic bilateral vagotomy. It is therefore possible that the hypothalamic feeding system is directly connected to autonomic systems influencing endocrine regulation of glucose ...
Primary cultures of chromaffin cells from bovine adrenal medulla were used as a model to evaluate the ability of 8-Br cyclic AMP (8-Br cAMP) to induce tyrosine hydroxylase (TH) and to study the role of cAMP-dependent protein kinase (cAPK) in this induction. This cell preparation maintains a constant level of cyclic nucleotides, catecholamines and related enzyme activities for about four weeks. Exposure of the cells for 5 hr to 8-Br cAMP produces, 48 hr later, a dose-related increase in the TH activity; 8-Br cGMP fails to modify TH. The increase in TH activity caused by 8-Br cAMP is due to an increase of the Vmax and is preceded by an activation of cytosol cAPK associated with a decrease of the total cytosol cAPK. A sustained increase in nuclear phosphorylation begins 8 to 12 hr after 8-Br cAMP application. The delayed increase in TH activity induced by 8-Br cAMP is blocked by actinomycin D, cycloheximide, colchicine and vinblastine. The reduction of the TH induction by colchicine and vinblastine ...
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TY - JOUR. T1 - Chlorpromazine and glucose metabolism. AU - Jori, A.. AU - Bernardi, D.. AU - Garattini, S.. PY - 1964/12. Y1 - 1964/12. N2 - Chlorpromazine in low doses (1.25 mg kg) reduces the tolerance to glucose load for more than 24 hr. The effect is not related to changes in body temperature and is present in both adrenalectomized and adrenal demedullated rats. Part of this effect of chlorpromazine is related to changes in permeability as shown by the decreased disappearance from blood stream of arabinose, a sugar which is not phosphorilated, after arabinose load.. AB - Chlorpromazine in low doses (1.25 mg kg) reduces the tolerance to glucose load for more than 24 hr. The effect is not related to changes in body temperature and is present in both adrenalectomized and adrenal demedullated rats. Part of this effect of chlorpromazine is related to changes in permeability as shown by the decreased disappearance from blood stream of arabinose, a sugar which is not phosphorilated, after ...
The Adrenal Glands are composed of two distinct parts, the adrenal medulla and the adrenal cortex. The adrenal medulla secretes two hormones Epinephrine and Norepinephrine in response to sympathetic stimulation. … ...
Cancer is often suspected from clinical signs. X-rays, ultrasound and MRI (magnetic resonance imaging) or CT (computerized tomography) scans may be useful in detecting the tumors, including metastases.. To identify the tumor type precisely, it is necessary to examine the tumor itself. This involves exploratory surgery, often with total removal of the tumor. After removal, the tissue samples are submitted for microscopic examination by histopathology. Specially prepared and stained tissue sections are made at a specialized laboratory where the slides will be examined by a veterinary pathologist.. The histopathology report typically includes words that indicate whether a tumor is benign (non-spreading, local growth) or malignant (capable of spreading to other body sites). These, together with the origin or type of tumor, the grade (degree of resemblance to normal cells or differentiation) and stage (how large it is and extent of spread) indicate how the cancer is likely to behave.. The ...
by competing in triathlons sits there trembling for a long time after the crisis has passed.. Does everyone in the restaurant suddenly suffer from "adrenal stress"? Absolutely. Do all 86 people need to be on herbal drugs "good for the adrenals" to prepare them for such adrenal stress? Absolutely not.. Quantitatively, the strength and duration of the adrenal stress response varies tremendously from one person to the next. But those who suffer ill effects during the 30 seconds of crisis and in the several minutes after it is clear the crisis has passed, are not victims of adrenal stress, but victims of whatever metabolic imbalance they carried with them into the restaurant.. A certain percentage of the people in that restaurant have a Sympathetic Imbalance - chronic catecholamine adrenal medulla stress. How do they respond to the frightening trauma of an assault right before their eyes? There is a tremendous outpouring of stress hormones, and those people will remain in a heightened state of ...
Plechners website offers a full explanation about adrenal medulla deficiency. With this immune endocrine imbalance, the IGA, IgG, and IgM all are weak. This weakness reduces the guts ability to absorb nutrients. According to Dr. Plechner, if the IGA is below fifty-eight, then animals cannot absorb their nutrients efficiently. And with the lack of an ability to take in the correct balance of nutrients, the animals ability to stay healthy is reduced. Over many months or years, the immune system progressively becomes more compromised. By balancing the gut with the right nutrients, MBRT, and giving the patient the added thyroid and/or adrenal support it needs, the immunoglobulins will become more normal and absorption of nutrients can occur. The laboratory evaluation for Plechner Syndrome can be done at Veterinary Diagnostic Services in Texas, and will give your practitioner the values. ...
When the body produces too much adrenaline, a person likely has phaeochromocytoma, a rare tumor of the adrenal medulla, according to the Society for Endocrinology. Symptoms of this condition include...
epinephrine: A hormone secreted by the adrenal medulla that is released into the bloodstream in response to physical or mental stress, as from fear or injury. It initiates many bodily responses, including the stimulation of heart action and an increase in blood pressure, metabolic rate, and blood glucose concentration.
Other Diseases in Children 13.1 Neuroblastoma Cause: Malignancy arising from cells of neural crest that form sympathetic ganglia and adrenal medulla Epidem: Most common malignant tumor of infancy (J Pediatr 1975;86:254). Accounts for 6-8% of all childhood malignancies; | 90% cases diagnosed in children | 5 yr (J Nucl Med 2004;45:1172). Most common primary site…
At the lateral edges of the neural plate, ridges appear that grow and fold towards each other to form a tube, the neural tube. The cells that lead this development are called Neural crest cells (C), and when they have completed their role in forming the neural tube, they go on to form some more specialised parts of the nervous system including the dorsal root ganglia, the autonomic nervous system and the adrenal medulla (D). ...
Summary of C16orf89 (MGC45438) expression in human tissue. Expression in several tissues, distinct in adrenal medulla and colloid staining in thyroid gland.
Expression of the noradrenaline transporter (NAT) was examined in normal human adrenal medulla and phaeochromocytoma by using immunohistochemistry and confocal microscopy. The enzymes tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) were used as catecholamine biosynthetic markers and chromogranin A (CGA) as a marker for secretory granules. Catecholamine content was measured by using high performance liquid chromatography (HPLC). In normal human adrenal medulla (n=5), all chromaffin cells demonstrated strong TH, PNMT and NAT immunoreactivity. NAT was co-localized with PNMT and was located within the cytoplasm with a punctate appearance. Human phaeochromocytomas demonstrated strong TH expression (n=20 samples tested) but variable NAT and PNMT expression (n=24). NAT immunoreactivity ranged from absent (n=3) to weak (n=10) and strong (n=11) and, in some cases, occupied an apparent nuclear location. Unlike the expression seen in normal human adrenal medullary tissue, NAT ...
Investigations into the effects of culturing bovine adrenal chromaffin cells in the presence (72 h) of dibutyryl cyclic AMP, forskolin, and reserpine on the level and release of [Met]enkephalyl-Arg6-Phe7 immunoreactivity, noradrenaline, and adrenaline are reported. The assay for [Met]enkephalyl-Arg6-Phe7 immunoreactivity recognises both peptide B, the 31-amino acid carboxy-terminal segment of proenkephalin, and its heptapeptide fragment, [Met]enkephalyl-Arg6-Phe7. Treatments that elevate cyclic AMP increase the amount of peptide immunoreactivity in these cells; this is predominantly peptide B-like immunoreactivity in both control cells and cyclic AMP-elevated cells. Treatment with reserpine gives no change in total immunoreactivity levels, but does not result in increased accumulation of the heptapeptide [Met]enkephalyl-Arg6-Phe7 at the expense of immunoreactivity that elutes with its immediate precursor, peptide B. Cyclic AMP treatment causes either no change or a decrease in levels of accumulated
Dopamine-ß-hydroxylase (DßH), an enzyme which catalyzes the conversion of dopamine to norepinephrine, is the only enzyme of the catecholamine biosynthetic pathway located in the chromaffin granules of adrenal medulla. Within the granules, two populations of DßH exist: a water-soluble fraction found within the granule matrix and a membrane-bound, amphiphilic fraction embedded in the surrounding bilayer. The amphiphilic form was purified to homogeneity following its extraction from the membrane with the non-ionic detergent BRIJ 58. Three steps were required to achieve complete purification: adsorption to ConA-Sepharose, adsorption to DEAE Sephadex A-25, and chromatography on Sephacryl S-200, Sepharose 6B, or Sepharose CL-4B. The presence of 0.1-0.2 mg/ml BRIJ 58 was essential for protein recovery. The enzymatic and structural characteristics of membrane-bound DßH were found to be similar to those of soluble DßH. Initial velocity data indicated a Ping-pong or double-displacement reaction with ...
S. Karanth, W. H. Yu, A. Walczewska, C. Mastronardi, S. M. McCann, Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide, Proceedings of the National Academy of Sciences, 2000, 97, 4, ...
Adrenal chromaffin cells (ACCs) secrete several neuroactive substances that are effective in influencing pain sensitivity in the central nervous system as well as enhancing the recovery of the intrinsic nigrostriatal dopaminergic system in patients w
TY - JOUR. T1 - Development of central control of adrenal catecholamine biosynthesis and release. AU - Slotkin, T. A.. AU - Chantry, Caroline J. AU - Bartolome, J.. PY - 1982. Y1 - 1982. N2 - In the mature rat, sympatho-adrenal Stressors evoke release of catecholamines from the adrenal medulla accompanied by stimulation of activity of catecholamine biosynthetic enzymes; both processes are controlled transsynaptically by impulses arising in the central nervous system. In the neonatal rat, drugs which ordinarily elicit sympatho-adrenal reflexes do not evoke neurally-mediated release and do not induce tyrosine hydroxylase or dopamine beta-hydroxylase, despite the fact that the central nervous system senses the stimuli and sends impulses down sympathetic preganglionic neurons; reflex responses first appear toward the end of the first week of postnatal life and are fully mature by 10 days of age. Since the immature adrenal medulla is capable of secreting catecholamines and inducing tyrosine ...
The sympathetic nervous system is activated by a variety of threats to organismal homeostasis. The adrenomedullary chromaffin cell is the core effector of sympathetic activity in the peripheral nervous system. By design, the chromaffin cell secretory response is mutable so that release can be rapidly tuned to drive context-dependent changes in physiological function. However, the mechanisms by which this tuning is achieved with such high temporal fidelity and context specificity remain unclear. This represents a major gap in our understanding of the sympatho-adrenal system since it is known to modify the function of nearly every organ system in the body. In chromaffin cells, the trigger for stimulus-evoked exocytosis is a rise in intracellular Ca2+. The level of intracellular Ca2+ accumulation varies with the stimulus intensity and secretagogue. Ca2+ regulates release by acting on the Ca2+-binding synaptotagmin (Syt) protein family, driving their penetration into membranes that harbor anionic lipids,