PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Adrenal Medulla”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Evidence for a plasma membrane calcium pump in bovine adrenal medulla but not adrenal cortex.

Continuous sucrose density gradient subfractions from bovine adrenal medullary microsomes were found to accumulate 45-Ca-2+ in the presence of ATP and ammonium oxalate mainly in subfractions of intermediate density. (Na-++K-+)-ATPase (plasma membrane marker) and Ca-2+-ATPase activities were also concentrated in these intermediate subfractions but thiamine pyrophosphatase (Golgi apparatus marker) was not. NADH oxidase (endoplasmic reticulum marker) activity was distributed throughout all subfractions. 45-Ca-2+ accumulation in adrenal cortical microsomes was found to rise and fall in parallel with thiamine pyrophosphatase but not with (Na-++K-+)-ATPase or NADH oxidase activities. Accumulation of 45-Ca-2+ in membrane vesicles in these experiments suggests the existence of a calcium transfer mechanism in plasma membranes of the adrenal medulla but not adrenal cortex.

Adenosine Triphosphatases↗
PubMed1979

Effects of muscle relaxants on catecholamine release from adrenal medulla.

Bovine adrenals were perfused with secretagogues in the presence or absence of muscle relaxants. On a molar basis, Dially-nor-toxiferine was as potent as tubocurarine in inhibiting the catecholamine release induced by carbachol; pancuronium was about 100 times less potent than tubocurarine, whereas gallamine and succinylcholine produced no inhibition whatsoever. KCl-induced catechoamine release was not affected by any of these compounds. Nicotine-induced catecholamine release was inhibitedby diallyl-nor-toxiferine, tubocurarine and pancuronium, but not by gallamine or succinylcholine. Muscarine failed to stimulate the adrenal medulla to release catecholamines. The results show that the inhibition of catecholamine release is based on the specific block of the nicotinic receptor, whereas gallamine and succinylcholine possess no blocking action, and that diallyl-nor-toxiferine and tubocurarine might affect clinical symptoms under conditions in which catecholamine release from the adrenal is increased by a compensatory mechanism.

Adrenal Medulla↗
PubMed1977

Stimulus-secretion coupling in chromaffin cells isolated from bovine adrenal medulla.

Bovine adrenal chromaffin cells were isolated by removal of the cortex and sequential collagenase digestion of the medulla. The catecholamine secretory function of these cells was characterized with respect to acetylcholine stimulation, cation requirements, and cytoskeletal elements. The dose-response curve for stimulated release had its half-maximum value at 10(-5) M acetylcholine, and maximum secretion was on the average 7 times that of control basal secretion. The differential release of epinephrine versus norepinephrine after stimulation with 0.1 mM acetylcholine occurred in proportion to their distribution in the cell suspension. The cholinergic receptors were found to be predominantly nicotinic. The kinetics of catecholamine release were rapid, with significant secretion occurring in less than 60 sec and 85% of maximum secretion within 5 min. A critical requirement for calcium in the extracellular medium was demonstrated, and 80% of maximum secretion was achieved at physiologic calcium concentrations. Stimulation by excess potassium (65 mM KCl) also induced catecholamine secretion which differed from acetylcholine stimulation in being less potent, in having a different dependence on calcium concentration, and in its response to the local anesthetic tetracaine. Tetracaine, which is thought to inhibit membrane cation permeability, was able to block acetylcholine-stimulated but not KCl-stimulated secretion. The microtubule disrupting agent vinblastine was able to block catecholamine release whereas the microfilament disrupter cytochalasin B had little effect. The results show the isolated bovine chromaffin cells to be viable, functioning, and available in large quantity. These cells now provide an excellent system for studying cell surface regulation of hormone and neurotransmitter release.

Adrenal Medulla↗
PubMed1975

Comparative effect of insulin and explanted adrenal medullary tissue and rat adrenal medulla in situ.

The adrenal medulla and explanted medullary cells in the anterior chamber of the eye were examined 3 h after the administration of insulin to rats. No alterations were seen in the explanted cells. In the adrenal medulla, light and electron microscopy indicated depletion of adrenaline cells; noradrenaline cells were not affected. Levels of catecholamines were three times higher in the explanted tissue after insulin treatment; in the medulla in situ they declined by 70%. These results confirm that insulin has no direct releasing effect on chromaffin cells.

Adrenal Medulla↗
PubMed1975

Further evidence for a cAMP dependent regulation of tyrosine-3-monoxygenase induction in adrenal medulla: effect of denervation.

Unilateral adrenal denervation caused a gradual decrease of adenylate cyclase activity in rat adrenal medulla. The extent of the increase in adrenal medullary 3',5'-cyclic adenosine monophosphate (cAMP) content elicited by injections of carbamylcholine declined gradually folling adrenal denervation. Three or nine days after denervation carbamylcholine caused rise of cAMP and a delayed increase of tyrosine-3-mono-oxygenase (TH) activity of similar magnitude in intact and denervated adrenal medullae. However, after an interval of 15 days or longer following denervation the increase in TH activity elicited by carbamylcholine was greatly reduced. These results support previous proposals that cAMP is involved as a second messenger in the trans-synaptic induction of TH.

Adenylyl Cyclases↗
PubMed1977

Catecholamine release from the adrenal medulla.

Chromaffin cells in the adrenal medulla are specialized for the synthesis, storage, and secretion of catecholamines. These cells are innervated by preganglionic sympathetic neurons in the splanchnic nerves, and, because of their unique blood supply, are exposed to unusually high concentrations of glucocorticoids in the venous drainage from the adrenal cortex. Splanchnic nerve stimulation appears to be the most important determinant of adrenomedullary function. Chromaffin cells synthesize catecholamines from tyrosine. Splanchnic nerve stimulation leads to an increase in the activity of several of the catecholamine biosynthetic enzymes, and to an increase in the rate of catecholamine biosynthesis. Glucocorticoids cause the induction of the enzyme noradrenaline N-methyltransferase, and so are particularly important for the synthesis of epinephrine. Catecholamines are stored, together with ATP, Ca2+, and protein, in secretory vesicles known as chromaffin granules. Splanchnic nerve stimulation is the physiological stimulus for catecholamine secretion. Stimulation of the splanchnic nerves results in the release of ACh from nerve endings in the adrenal medulla. ACh causes an increase in the permeability of the chromaffin cells to Ca2+, and thereby leads to the entry of Ca2+ into the cells. Ca2+ then causes the secretion of catecholamines and of other chromaffin granule constituents from the chromaffin cells by exocytosis. The biochemical mechanisms of exocytosis, and the mechanism by which Ca2+ stimulates this process, are still unknown.

Acetylcholine↗
PubMed1979

Mechanism of PGE inhibition of catecholamine release from adrenal medulla.

Catecholamine (CA) secretion from the adrenal medulla was induced in vitro by acetylcholine (10(-4)M) (ACh), by incubation in potassium-free medium, by addition of ouabain (10(-3)M), by theophylline (10(-2)M) or by salbutamol (10(-6) and 6 x 10(-6) M). Theophylline and salbutamol, but not ACh, released CA in a calcium-free medium supplemented with 2mM EGTA. PGE2 significantly inhibited both CA secretion evoked by ACh and that evoked by salbutamol, i.e. both secretion dependent on, and independent of, extracellular calcium, PGE2 counteracted the increase of cAMP levels caused by ACh or salbutamol in adrenal medullary slices. PGE2 also diminished the salbutamol-induced activation of adenylate cyclase in an adrenal medullary membrane preparation, PGE2 reduced the rate of 45Ca efflux from slices of adrenal medulla preloaded with 45CaCl2. It is suggested that PGE2 inhibits CA secretion through the following sequence: inhibition of adenylate cyclase, a fall of cellular cAMP resulting in reduced release of calcium from intracellular binding sites and reduced free cytoplasmic calcium.

Adenylyl Cyclases↗
PubMed1975

Tissue specificity of nuclear acidic proteins isolated from bovine brain and adrenal medulla.

Nuclear acidic proteins from bovine brain and adrenal medulla demonstrated dissimilar electophoretic and chemical profiles. The amino acid analysis of the acidic nuclear protein fraction isolated from these tissues revealed some variation in the ratio of acidic to basic amino acids. The estimation of free carboxylic acid groups confirmed the more acidic nature of the brain proteins. In comparing the acrylamide gels either visually or optically, several electrophoretically specific bands were apparent. Although the total number of protein bands from each tissue was approximately the same, the adrenal medulla contained a larger proportion of the more positively charged proteins. These observations are interpreted to indicate that the nuclear acidic protein from brain and adrenal medulla may show functional variation.

Adrenal Medulla↗
PubMed1979

Effects of methoxyverapamil on the stimulation by Ca2+, Sr2+ and Ba2+ and on the inhibition by Mg2+ of catecholamine release from the adrenal medulla.

1 Bovine adrenal glands were perfused with Ca2+-free Locke solution and catecholamine release was induced either by the introduction of Ca2+, Sr2+ or Ba2+ into the perfusion fluid or by the substitution of Na+ by an osmotically equivalent amount of sucrose. 2 Methoxyverapamil (D600) at a concentration of 3 X 10(-4) M blocked the release of catecholamines in response to Ca2+, Sr2+ or Ba2+ stimulation but failed to block the release evoked by the omission of Na+. 3 Mg2+ (10 to 20 mM) blocked the release induced by Na+-deprivation; however, this inhibitory effect of Mg2+ was not modified by D600. 4 D600 blocked the increase in the efflux of 45Ca from the perfused gland induced by the introduction of Ca2+ into the perfusion fluid and blocked the uptake of 45Ca into adrenal medullary slices induced by K+ depolarization. 5 The results suggest that Ca2+, Sr2+ and Ba2+ may enter the chromaffin cell through the same channel and that this channel is blocked by D600. Mg2+ may enter the cell through the same Ca2+ channel but with a high rate of permeation or it may enter through a channel which is resistant to D600. Alternatively, Mg2+ may exert this inhibitory effect at an extracellular site.

Adrenal Medulla↗
PubMed1977

Tyrosine hydroxylase: delayed activation in central noradrenergic neurons and induction in adrenal medulla elicited by stimulation of central cholinergic receptors.

The centrally active muscarinic agonist, oxotremorine, elicited an up to 2-fold dose-dependent (0.25-1.5 mg/kg) increase in the activity of tyrosine hydroxylase (TH) in the rat nucleus locus coeruleus (LC) and adrenal medulla. The response occurred in LC after 24 to 48 hours and in adrenal medulla by 4 to 8 hours, peaked in LC at 72 hours and adrenal medulla at 16 to 24 hours and persisted up to 2 weeks in both tissues. In brain the effect appeared confined to cell bodies of noradrenergic neurons. The activity of dopamine beta-hydroxylase increased in adrenal medulla (40%) but not in brain. Immunotitration with anti-TH serum demonstrated that the increase of TH activity in LC is due to increased catalytic activity (activation), whereas in adrenal medulla it is due to a transynaptically mediated accumulation of enzyme protein (induction). Physostigmine (1.0 mg/kg), pilocarpine (25-50 mg/kg) and nicotine (10 mg/kg) increased TH activity in LC and adrenal. We conclude that stimulation of central cholinergic receptors of the muscarinic type results in a delayed and protracted activaiton of TH but not of dopamine beta-hydroxylase in cell bodies of central noradrenergic neurons, and reflexly, to transynaptic induction of TH and dopamine beta-hydroxylase in the adrenal medulla.

Adrenal Medulla↗
PubMed1977

Acetylcholine and cAMP in adrenal medulla:indirect effect.

Catecholamine release and cAMP accumulation were studied in bovine adrenal medulla slices in vitro. Acetylcholine (10(-4) M) and salbutamol (10(-6) M) caused increased release of catecholamines and accumulation of cAMP. Incubation in Ca2+ -free medium abolished the release of catecholamines and the increase of cAMP caused by acetylcholine but not that caused by salbutamol. In a membrane fraction of adrenal medulla acetylcholine (10(-4) M) had no effect on adenylate cyclase activity but salbutamol (10(-6) M) caused substantial activation of adenylate cyclase. It is suggested that acetylcholine has no direct effect on adenylate cyclase or cAMP in adrenal medulla and the accumulation of cAMP observed in slices incubated with acetylcholine is due to the effect of catecholamines, released by acetylcholine, on the medullary cells.

Acetylcholine↗
PubMed1977

Selective induction of tyrosine hydroxylase and dopamine beta-hydroxylase by nerve growth factor: comparison between adrenal medulla and sympathetic ganglia of adult and newborn rats.

Administration of NGF to newborn and adult rats elicits a selective increase in TH and DBH both in sympathetic ganglia and adrenal medulla. This effect does not depend on intact preganglionic cholinergic fibers. The augmented enzyme activity results from enhanced enzyme synthesis since it can be abolished by cycloheximide and NGF has been shown to enhance the incorporation of [3H]leucine into DBH molecules. The responsiveness of the adrenal medulla to NGF is also supported by light and electron microscopic autoradiograms which show that intravenously injected 125I-NGF is accumulated with high selectivity in adrenal chromaffin as compared to adjacent adrenal cortical cells. In spite of the many similarities between the response of the adrenergic neurons and adrenal chromaffin cells to NGF, there are also two distinct differences. (a) In newborn rats the ratio between the TH increase effected by a single and 10 subsequent daily injections of NGF is 1:2 in the adrenal medulla and 1:7 in the superior cervical ganglia. (b) If adrenal medullae are transferred to organ culture after intravenous injection of NGF, maximal TH response is initiated 60-90 min after NGF administration. In superior cervical ganglia only a half-maximal response is initiated at that time. After a stationary phase a second increase starts after about 6 h to reach the maximum after 12 h. The biphasic time course of the initiation of TH induction by NGF in sympathetic ganglia is in agreement with the time course of 125I-NGF accumulation after intravenous injection27 reflecting the moiety of NGF reaching the cell bodies of the adrenergic neurons directly by the blood stream (initial accumulation) and by retrograde axonal transport (second phase).

Adrenal Medulla↗
PubMed1975

Protein kinase activation as an early event in the trans-synaptic induction of tyrosine 3-monooxygenase in adrenal medulla.

An increase of cAMP/cGMP concentration ratio is the earliest stimulus-coupled biochemical change that has been measured in the adrenal medulla during the trans-synaptic induction of tyrosine 3-monooxygenase [EC 1.14.16.2; L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating)]. In adrenal medulla of rats receiving reserpine alone (16 mumol/kg intraperitoneally) or reserpine and propranolol (40 mumol/kg intraperitoneally 30 min before reserpine), or exposed to 4 degrees for 4 hr, the extent and duration of the increase of the cAMP/cGMP concentration ratio exceeds the critical value that is required to activate the protein kinases (EC 2.7.1.37; ATP:protein phosphotransferase). Gel filtration experiments indicate that during this activation, the catalytic subunit of the protein kinase (low-molecular-weight enzyme) is released from the holoenzyme. The activation of protein kinase lasts longer than the increase in the cAMP/cGMP concentration ratio and appears to be an obligatory early event that mediates the increase of tyrosine monooxygenase synthesis. The trans-synaptic induction of the monooxygenase in adrenal medulla appears to be due to an increased synthesis of the enzyme;the rate for monooxygenase degradation is proportional to the number of enzyme molecules that are present at various stages of the induction process.

Adrenal Medulla↗
PubMed1977

Ultrastructural cytochemistry of the human adrenal medulla.

A cytochemical study of the human adrenal medulla showed that it is made up of two types, the adrenaline (A-) and noradrenaline (N-) storing cells. A-and N-storing granules were argentaphobic when ultra-thin sections of Araldite-embedded medulla were stained according to the periodic acid-thiocarbohydrazide silver proteinate technique of Thiery. A small amount of glycogen (which disappeared after digestion with alpha amylase) in the form of B-particles, as well as lysosomes were, however, visualized by this technique. The entire core of A granules was markedly positive after ultrathin sections of glutaraldehyde-fixed, glycol methacrylate (GMA-) embedded medullae were stained with phosphotungstic acid (PTA) at a low pH (O.3). The N granules, in contrast, were mostly unreactive. PTA stained a large part of the Golgi complex of A cells, whereas it generally had no such effect on that of the N cells. In both cell types, the cell coat, lysosomes and multivesicular bodies reacted to PTA. The periodic acid schiff (PAS) technique showed A but not N granules in semithin sections of GMA-or Araldite-embedded medullae. The PTA and PAS stains were abolished by acetylation, restored by saponification, unchanged by methylation and greatly diminished by sulfation or by digestion with beta glucuronidase after oxidation by perchloric acid. These results indicate that in man the A granules and the Golgi complex of A cells, unlike the same structures in N cells, are rich in glycoproteins.

Adrenal Medulla↗
PubMed1976

Association between the increase of cAMP content and the trans-synaptic induction of tyrosine hydroxylase in rat adrenal medulla. Studies with dexamethasone and reserpine.

When dexamethasone 0.25 or 2.5 mumole/kg i.p. was injected 2 h before reserpine (16 mumol/kg i.p.) the time course of the increase in cAMP content of rat adrenal medulla was changed. Reserpine alone caused a monophasic increase lasting between 1-2 h; reserpine after dexamethasone caused a biphasic increase: the immediate response, lasting between 15 and 30 min, was followed by a secondary increase beginning 2-3 h after reserpine and lasting for several hours. The overall increase in cAMP content elicited by reserpine during the 8 h following injection remained unchanged or was even increased, depending on the dose of dexamethasone. Pretreatment with dexamethasone, which delayed the increase in cAMP, also delayed the activation and translocation of protein kinase and the induction of tyrosine hydroxylase caused by reserpine in adrenal medulla. The action of reserpine on the cAMP content of adrenal medulla required an intact innervation and did not appear to be related to increased secretion of ACTH from pituitary. In denervated adrenals reserpine failed to increase the cAMP content of the medulla but not that of the cortex.

Adrenal Cortex↗
PubMed1979

Appearance of tyrosine hydroxylase, aromatic amino-acid decarboxylase, dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase during the ontogenesis of the adrenal medulla: an immunohistochemical study in the rat.

The cellular localization of the enzymes tyrosine hydroxylase (TH), aromatic amino-acid decarboxylase (or dopa decarboxylase, DDC), dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) in the adrenal medulla of adult rats and rat fetuses (14th, 17th, 18th, 19th and 21st day) was examined. In the prenatal stages the medullary blastema and an adjacent part of the primitive sympathetic trunk were also investigated. Tissues were fixed in ice-cold 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.2). Cryostat sections (10 micron in thickness) were stained by the indirect immunofluorescence technique. Rabbit antibodies to TH (isolated from human pheochromocytoma), DDC, DBH and PNMT (the latter three isolated from bovine adrenal medulla) were used. Sections incubated with serum of non-immunized rabbits were used as controls. In the adult adrenal medulla, two cell types can be distinguished. One cell type contains only TH, DDC and DBH. The other cell type contains PNMT in addition. It is concluded that these cells correspond to the noradrenaline-(NA-) and adrenaline- (A-)storing cells respectively. In all prenatal stages TH, DDC and DBH are found in the primitive sympathetic trunk, in the medullary blastema, and in the medullary cells which have migrated into the cortical "anlage". PNMT is observed for the first time on the 18th day. Moreover, PNMT could only be demonstrated inside the adrenal gland. From these observations it is concluded that the capacity to synthesize NA is developed even before the "medullary" cells have reached the cortical "anlage". On the contrary, the capacity to synthesize A seems to be acquired only after this contact is established. The hypothesis is put forward that this phenomenon might indicate the induction of PNMT by glucocorticoids secreted by the fetal cortex.

Adrenal Medulla↗
PubMed1978

Different types of small granule-containing cells and neurons in the guinea-pig adrenal medulla.

An electron microscopic, histo- and biochemical study was carried out on the adrenal medulla of newborn and adult guinea-pigs giving special emphasis to small granule-containing (SGC) cells. Adrenaline (A) was the predominating catecholamine (CA) both in newborn (70-90% of total CA) and adult (85-90%) guinea-pig adrenals. In analogy to the biochemical findings electron microscopy revealed a high predominance of A cells, which contained large granular vesicles with an average diameter of 180 nm. Most noradrenaline (NA) storing cells showed granular vesicles of a considerably smaller average diameter (80 nm) and had a higher nuclear-cytoplasmic ratio. These cells were termed SGC-NA cells. NA cells with large granular vesicles (average diameter 170 nm) were extremely rare. Another type of SGC cells contained granular vesicles with cores of low to medium electron-density (SGC-NA-negative cells). Biochemical determinations made it unlikely that these cells contained predominantly dopamine (DA). SGC cells were scarcely innervated by cholinergic nerves. They formed processes, which were found both in the adrenal cortex and medulla contacting blood vessels including sinusoid capillaries, steroid producing cells of the reticularis and fasciculata zone and processes, which were interpreted to belong to medullary nerve cells. Two types of neurons were present in the guinea-pig adrenal medulla, one resembling the principal neurons in sympathetic ganglia, the other, which, principal neurons and SGC cells. In adrenomedullary grafts under the kidney capsule, which were studied three weeks after transplantation, "ordinary" A cells resembled SGC-NA negative cells with respect to their ultramorphology. Processes of transplanted principal neurons showed uptake of 5-hydroxydopamine and, hence, were considered to be adrenergic. Despite the lack of extrinsic nerves to the transplants, few principal neurons received cholinergic synapses, the origin of which is uncertain to date.

Adrenal Medulla↗