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PubMed2006

Corticotropin-releasing factor (CRF) and the urocortins differentially regulate catecholamine secretion in human and rat adrenals, in a CRF receptor type-specific manner.

Corticotropin-releasing factor (CRF) affects catecholamine production both centrally and peripherally. The aim of the present work was to examine the presence of CRF, its related peptides, and their receptors in the medulla of human and rat adrenals and their direct effect on catecholamine synthesis and secretion. CRF, urocortin I (UCN1), urocortin II (UCN2), and CRF receptor type 1 (CRF1) and 2 (CRF2) were present in human and rat adrenal medulla as well as the PC12 pheochromocytoma cells by immunocytochemistry, immunofluorescence, and RT-PCR. Exposure of dispersed human and rat adrenal chromaffin cells to CRF1 receptor agonists induced catecholamine secretion in a dose-dependent manner, an effect peaking at 30 min, whereas CRF2 receptor agonists suppressed catecholamine secretion. The respective effects were blocked by CRF1 and CRF2 antagonists. CRF peptides affected catecholamine secretion via changes of subplasmaliminal actin filament polymerization. CRF peptides also affected catecholamine synthesis. In rat chromaffin and PC12 cells, CRF1 and CRF2 agonists induced catecholamine synthesis via tyrosine hydroxylase. However, in human chromaffin cells, activation of CRF1 receptors induced tyrosine hydroxylase, whereas activation of CRF2 suppressed it. In conclusion, it appears that a complex intraadrenal CRF-UCN/CRF-receptor system exists in both human and rat adrenals controlling catecholamine secretion and synthesis.

Adrenal Glands↗
PubMed2005

Catecholamines' enhancement of inducible nitric oxide synthase-induced nitric oxide biosynthesis involves CAT-1 and CAT-2A.

Catecholamines enhance inducible nitric oxide synthase (iNOS) expression that results in nitric oxide (NO) overproduction in lipopolysaccharide (LPS)-stimulated macrophages. L-arginine transport mediated by cationic amino acid transporters (including CAT-1, CAT-2, CAT-2A, and CAT-2B) is crucial in regulating iNOS activity. We sought to assess the effects of catecholamines on L-arginine transport and CAT isozyme expression in stimulated macrophages. Confluent RAW264.7 cells were cultured with LPS with or without catecholamines (epinephrine or norepinephrine, 5 x 10(-6) M) for 18 h. NO production, L-arginine transport, and enzyme expression were determined. Our data revealed that LPS co-induced iNOS, CAT-2, and CAT-2B expression, whereas CAT-1 and CAT-2A expression remained unaffected. Significant increases in NO production and L-arginine transport (approximately eight-fold and three-fold increases, respectively) were found in activated macrophages. Catecholamines significantly enhanced NO production and L-arginine transport (approximately 30% and 20% increases, respectively) in activated macrophages. Catecholamines also enhanced the expression of iNOS, CAT-1, and CAT-2A but not CAT-2 or CAT-2B in LPS-stimulated macrophages. Furthermore, the enhancement effects of catecholamines were inhibited by either dexamethasone or propranolol. We provide the first evidence to indicate that L-arginine transport in activated macrophages could be enhanced by catecholamines. Furthermore, this catecholamine-enhanced L-arginine transport might involve CAT-1 and CAT-2A but not CAT-2 or CAT-2B.

Animals↗
PubMed2000

The effects of acute hypoxia on chemically or neuronally induced catecholamine secretion in rainbow trout (Oncorhynchus mykiss) in situ and in vivo.

The potential direct and modulating effects of acute hypoxia on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in situ, using a perfused cardinal vein preparation, and in vivo, using chronically cannulated fish. Acute (10 min) perfusion with hypoxic (P(O2)<10 mmHg) saline or homologous hypoxic blood did not have a statistically significant effect on basal (non-stimulated) catecholamine secretion. A field stimulation technique was used to excite the sympathetic nerves innervating the chromaffin cells electrically in situ under conditions of high-P(O2) (saline P(O2)=152 mmHg; 1 mmHg=0.133 kPa) or low-P(O2) (saline P(O2)<10 mmHg) perfusion at constant P(CO2) (2.3 mmHg). The results demonstrated that neuronally evoked catecholamine secretion was significantly lowered by 50 % during perfusion with hypoxic saline. To assess whether the inhibitory effect of hypoxia during neuronal stimulation in situ resulted from modulation of nicotinic and/or muscarinic receptor-linked pathways, perfused posterior cardinal vein preparations were injected with selective nicotinic (10(-)(7) or 10(-)(6 )mol kg(-)(1) nicotine) or muscarinic (10(-)(3 )mol kg(-)(1) methacholine) receptor agonists. For both doses of nicotine, catecholamine secretion was significantly lowered during hypoxia by 55 %. During muscarinic receptor stimulation, perfusion with hypoxic saline caused a 42 % reduction in the rate of catecholamine secretion. In contrast, catecholamine secretion elicited by depolarising levels of KCl (60 mmol l(-)(1)) was unaffected by the oxygen status of the perfusate. In vivo, intra-arterial injections of nicotine (300-600 nmol kg(-)(1)) into normoxic (water P(O2)=155 mmHg) or moderately hypoxic fish (water P(O2)=80 mmHg) caused a dose-dependent elevation of circulating catecholamine levels. However, despite the inhibitory influence of localised hypoxia on chromaffin cell responsiveness previously demonstrated in situ, the increase in plasma catecholamine levels after intra-arterial injection of nicotine was significantly enhanced in the hypoxic fish. The differences between the results from the in vivo and in situ experiments may reflect the contribution of higher control centres and modulating factors in vivo that are absent in situ.

Animals↗
PubMed1978

Differential effects of D 600 on release of catecholamines by acetylcholine, histamine, tyramine and by cyclic AMP from canine adrenal medulla.

The isolated canine adrenal glands were perfused retrogradely with Locke's solution, and the catecholamine contents of the effluents were measured by the trihydroxyindole-fluorimetric method. Stimulation of the glands by acetylcholine, histamine, tyramine and cyclic AMP caused an increase in release of catecholamines from the glands. Introduction of D 600 of the perfusion medium reduced release of catecholamines in response to acetylcholine, and this reduction was overcome by raising calcium ion concentrations of the perfusion medium. Similarly, D 600 reduced release of catecholamines in response to histamine. The release of catecholamines evoked by tyramine was also inhibited by D 600, although to a lesser degree than the release by acetylcholine. In contrast, D 600 was entirely ineffective on the catecholamine release in response to cyclic AMP. D 600 had no effect on the spontaneous catecholamine output. From these results it was concluded that release of catecholamines from adrenal chromaffin cells by acetylcholine and histamine, and by tyramine in part requires the entry of calcium ions across the cell membane, whereas that by cyclic AMP does not.

Acetylcholine↗
PubMed2003

Catecholamine-synthesizing enzymes in carcinoid tumors and pheochromocytomas.

BACKGROUND: Serotonin is the principal endocrine product of carcinoid tumors, but simultaneously increased production of catecholamines has been described in these tumors. As it is not clear whether these tumors contain specific enzymes for catecholamine synthesis, we aimed to detect catecholamine-synthesizing enzymes [tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH), and phenylethanolamine-N-methyltransferase (PNMT)] in midgut carcinoid tumors and pheochromocytoma and to correlate enzyme expression to serotonin production as well as catecholamines and metabolites excreted in urine. METHODS: Paraffin-embedded tumor specimens from 21 midgut carcinoid patients and 20 pheochromocytoma patients (10 sporadic and 10 MEN type IIa-related tumors) were stained for TH, DBH, and PNMT, using a three-step biotin-avidin-peroxidase method. RESULTS: TH was demonstrated in 9 (43%) of 21 carcinoids and in all (100%) of 20 pheochromocytomas, DBH in 8 (38%) carcinoids and in 15 (75%) pheochromocytomas, and PNMT in 7 (33%) carcinoids and in 13 (65%) pheochromocytomas. Increased urinary excretion of catecholamines and metabolites was observed in 10 (48%) carcinoid patients and in all pheochromocytoma patients. No clinically relevant association between enzyme expression and urinary excretion of catecholamines and metabolites was found. CONCLUSIONS: Catecholamine-synthesizing enzymes are present in many carcinoid tumors. This finding possibly indicates the existence of a catecholamine-synthesizing pathway in carcinoids similar to that found in pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1988

Plasma free and sulfoconjugated catecholamines during acute asphyxia in the sheep fetus--relation to cardiovascular parameters.

Changes of free and sulfoconjugated catecholamines were measured radioenzymatically during a 5 minute period of acute asphyxia in chronically instrumented sheep fetuses (n = 5). Due to total reduction of uterine blood flow asphyxia as well as metabolic acidosis developed (pH = 6.94 +/- 0.02; Pco2 = 98 +/- 8 mmHG; lactate = 7.1 +/- 0.3 mmol/l). Peak concentrations of free catecholamines were reached after 3 minutes; free NE increased 60-fold, free E 370-fold and free DA 13-fold as compared to control values. Concomitantly, sulfoconjugated catecholamines rose markedly and were 40-fold (NE), 300-fold (E) and 10-fold (DA) higher when compared to the control period. Thus, the results reveal that the fetal sulfoconjugating system is very effective and able to match high concentrations of free catecholamines entering the circulation. After release of occlusion, free and sulfoconjugated catecholamines decreased with a half life time of 2.5 to 4.3 minutes during the initial 10 minutes. A close correlation could be demonstrated between free catecholamines and fetal arterial blood pressure, however, with interference of the effects of desoxygenation on the myocard. Moreover, fetal tachycardia is related to circulating catecholamines, especially E, during the postasphyxial period. Our results suggest, that in unstressed, normoxic fetuses the cardiovascular system is able to maintain basic functions (heart rate and blood pressure) during asphyxia for 5 minutes. In this context, a maximal sympathoadrenal stimulation with secretion of free catecholamines seems to be essential.

Acute Disease↗
PubMed1994

Decreased adrenal medullary catecholamine release in spontaneously diabetic BB-Wistar rats. Role of hypoglycemia.

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 defect in catecholamine secretion was also seen in adrenals harvested from nondiabetic BB-Wistar rats following a 3-h period of acute hypoglycemia; however, the adrenal response to potassium was also decreased as was the catecholamine content of the adrenal. Conversely, nondiabetic BB-Wistar rats made diabetic with streptozocin (STZ) and maintained in a hyperglycemic state did not exhibit catecholamine hyposecretion 2 weeks after STZ administration. Collectively, the data describe decreased adrenomedullary response to cholinergic stimulation in spontaneously diabetic rats as early as 2 weeks after the onset of diabetes and that a similar, although more severe, hyposecretion occurs after acute, severe hypoglycemia.

Acetylcholine↗
PubMed1978

Effect of nicotinic acid on catecholamine synthesis in rat brain.

Effect of nicotinic acid on the formation of catecholamine has been studied. Norepinephrine and dopamine concentrations in brain were 30 per cent higher and brain catecholamine formation was 50 per cent higher in the nicotinic acid-supplemented rats than the nicotinic acid-deficient rats. However, these catecholamine levels of the nicotinic acid-deficient rats were recovered by the administration of nicotinic acid. The concentration of brain tyrosine was unaltered after administration of nicotinic acid to the nicotinic acid-deficient rats. Therefore, the changes catecholamine formation by the nicotinic acid supplementation were not due to the difference of tyrosine concentration in the brain which is the precursor for catecholamine biosynthesis. As the difference of catecholamine concentration between the nicotinic acid deficient and the nicotinic acid supplemented group was smaller than that of catecholamine formation of these groups, the turnover of catecholamine was supposed to be decreased in nicotinic acid deficiency.

Animals↗
PubMed1999

Functional involvement of angiotensin AT2 receptor in adrenal catecholamine secretion in vivo.

The aim of the present study was to analyse modulations of adrenal catecholamine secretion from the adrenal gland of anesthetized dogs in response to locally administered angiotensin II (AngII) in the presence of either PD 123319 or CGP 42112, both of which are highly specific and selective ligands to angiotensin AT2 receptor. Plasma concentrations of epinephrine and norepinephrine in adrenal venous and aortic blood were quantified by a high performance liquid chromatography coupled with electrochemical detection (HPLC-EC) method. Adrenal venous blood flow was measured by gravimetry. Local administration of AngII (0.05 microg, 0.1 microM) to the left adrenal gland increased adrenal gland catecholamine output more than 30 times that found in nonstimulated states. Administration of either PD 123319 (0.085 microg (0.23 microM) to 8.5 microg (23 microM)) or CGP 42112 (0.005 microg (0.01 microM) to 5 microg (10 microM)) did not affect the basal catecholamine output significantly. The increase in adrenal catecholamine output in response to AngII was inhibited by approximately 80% following the largest dose of PD 123319. CGP 42112 significantly attenuated the catecholamine response to AngII by approximately 70%. PD 123319 and CGP 42112 were devoid of any agonist actions with respect to catecholamine output by the adrenal gland in vivo. Furthermore, both PD 123319 and CGP 42112 inhibited the increase in adrenal catecholamine secretion induced by local administration of AngII. The present study suggests that AT2 receptors play a role in mediating catecholamine secretion by the adrenal medulla in response to AngII receptor agonist administration in vivo.

Adrenal Glands↗
PubMed1999

Glucose does not affect catecholamine stimulus-secretion coupling in rat adrenal medulla: relationship to low changes in osmolarity and to insulin.

Glucose levels were analyzed to see whether they directly affect the catecholamine release from chromaffin cells. We incubated isolated adrenal medullae of rats in Krebs-Hepes modified solutions with several glucose concentration, in the presence and absence of carbachol or insulin. Transfer of the medulla from a solution with 11.1 mM of glucose to a 0.56 mM one caused an increase in catecholamine secretion. Relative increase in change of glucose levels from 25 to 0.56 mM and from 50 to 0.56 mM enhanced the effect mentioned above. An inhibitory effect was detected after transfer of the medulla from 0.56 mM to 50 mM glucose. However, correction of solution osmolarity with mannitol or NaCl switched back catecholamine secretion to basal levels in all groups, and correction of solution osmolarity with sucrose indicated an impairment of catecholamine release. No difference was observed in stimulated catecholamine secretion (100 microM of carbachol) at all glucose levels. Further, the presence of insulin did not affect catecholamine secretion in all groups. Our results suggest that in isolated adrenal medullae of rats (1) glucose or variations in glucose levels do not affect catecholamine released; (2) isolated adrenal medulla of rat was highly sensitive to hyperosmolarity and extremely sensitive to hyposmolarity; (3) Insulin had no acute direct effect on catecholamine secretion in isolated adrenal medullae of rats.

Adrenal Medulla↗
PubMed1991

Heart and catecholamines.

Catecholamines mediate their effects in the heart through beta 1- and beta 2-receptors. Beta 1-receptors mediate the effects of sympathetic nerve stimulation. Alpha-receptors may have a role but, unlike the beta-receptor mediated responses, act without producing any increase in cyclic AMP. Prolonged receptor stimulation results in a reduction in beta-receptor sensitivity. In contrast blockade with a non-agonist agent is associated with an increase in catecholamine sensitivity which may be responsible for the withdrawal reactions that can occur when beta-blocking drugs are rapidly withdrawn in patients with ischaemic heart disease. Experimentally, prolonged noradrenaline infusions result in ventricular hypertrophy. Catecholamines have been implicated in several pathologies. High and rising catecholamine levels are associated with worsening of prognosis in patients with heart failure. These patients show a decreased beta-receptor number and cellular concentration of catecholamines. On the other hand cardiomyopathy is associated with an increased sensitivity to catecholamines. Catecholamines aggravate cardiac damage in ischaemia. Excessively high catecholamine loads cause myocardial damage in otherwise normal hearts, for example in patients with a phaeochromocytoma and those with various forms of cerebral damage such as subarachnoid haemorrhage, cerebrovascular accidents, and head injury.

Adrenergic beta-Antagonists↗
PubMed1991

Advances in catecholamine and metabolite measurements for diagnosis of pheochromocytoma.

Assessment of catecholamine production and excretion is important in the laboratory detection of pheochromocytoma, a rare but curable cause of hypertension. Advances in catecholamine and metabolite methodologies have enhanced the diagnostic acumen by increasing analytical sensitivity and eliminating many of the interferences observed with earlier methods. Estimation of urinary catecholamines metanephrine and vanillylmandelic acid is routinely used in the biochemical detection of pheochromocytoma and in monitoring the completeness of tumor excision as well as the possibility of recurrence. Traditional spectrophotometric and fluorometric methods for urinary catecholamines and their metabolites are being replaced by highly sensitive and selective chromatographic methods. The ability to quantify individual catecholamines and metanephrines by high-performance liquid chromatography is of particular value for detecting familial forms of the tumor that may secrete epinephrine. Plasma norepinephrine and epinephrine measurements are of additional diagnostic value in determining recent catecholamine release and response to clonidine suppression. For either urine or plasma measurements, appropriate patient preparation, sample collection, and method validation along with an understanding of the variable pattern of catecholamine secretion and metabolism in pheochromocytoma are essential. Advances in laboratory methodology and reference intervals for catecholamines for clinical interpretation are reviewed.

Adrenal Gland Neoplasms↗
PubMed1991

Catecholamine concentrations in plasma and organs of the fetal guinea pig during normoxemia, hypoxemia, and asphyxia.

To examine the responses of the sympatho-adrenal system to reduced oxygen supply we studied plasma and tissue concentrations of catecholamines during normoxemia, hypoxemia, and asphyxia in 22 fetal guinea pigs near term. Fetal blood was obtained by cardiopuncture in utero under ketamine/xylazine-anesthesia. Catecholamines were determined in plasma and tissue of 15 organs and 14 brain parts by HPLC-ECD. During normoxemia (SO2 54 +/- 4 (SE) %, pH 7.36 +/- 0.02, n = 5) plasma catecholamine levels were low (norepinephrine 447 +/- 53, epinephrine 42 +/- 12, dopamine 44 +/- 6 pg/ml). During hypoxemia (SO2 27 +/- 3%, pH 7.32 +/- 0.01, n = 6) and asphyxia (SO2 24 +/- 2%, pH 7.23 +/- 0.02, n = 11) tissue catecholamine concentrations changed with changing blood gases and with increasing plasma catecholamines. Norepinephrine concentrations increased in both skin and lung and decreased in liver, pancreas, and scalp; those of epinephrine increased in the heart, lung liver, and scalp and decreased in the adrenal. There were only minor changes in brain catecholamine concentrations except for a 50% reduction in dopamine in the caudate nucleus. Concentrations of dopamine catabolite 3,4-dihydroxyphenylacetic acid decreased in many brain parts, suggesting that cerebral catecholamine metabolism was affected by hypoxemia and asphyxia. We conclude that the sympatho-adrenal system of fetal guinea pigs near term is mature and that its stimulation by reduced fetal oxygen supply leads to changes in both plasma and tissue catecholamine concentrations.

Acid-Base Equilibrium↗
PubMed1991

Catecholamine levels in pregnant physicians and nurses: a pilot study of stress and pregnancy.

As a pilot study of occupational stress and pregnancy, we measured urinary catecholamine excretion in ten pregnant physicians and three intensive care nurses between 26-37 weeks' gestation, once during a work day and again during a non-work day. Urinary catecholamines were increased by 58% (P less than .03) during work periods compared with non-work periods. Catecholamine levels were also increased by 64% (P less than .025) over those of a working non-physician control group of similar gestational age. Urinary catecholamine levels are a direct reflection of plasma catecholamine levels. Catecholamine levels are known to increase with physical stress, such as standing, and with mental stress, such as difficult problem-solving. Catecholamines are also known to decrease uterine blood flow. Measurement of catecholamines may be a helpful marker in investigating the relationship between occupation and pregnancy outcome.

Catecholamines↗
PubMed1990

Conjugated catecholamines in human plasma: where are they coming from?

The origins of conjugated catecholamines remain poorly known. The aim of the present study was to see whether a major contribution comes from the sympathetic nervous system. We have assumed some kind of parallelism between the activity of the sympathetic nervous system, the amount of catecholamines released and taken up, and the amount of conjugated catecholamines circulating in plasma. Accordingly, an increase in sympathetic activity should be followed by an increase in the plasma level of conjugated catecholamines. The plasma levels of sulfoconjugated and glucuroconjugated catecholamines were measured in 10 patients with mental disease resistant to drug treatment, before and after electroconvulsive therapy. As expected, blood pressure, norepinephrine concentration, and epinephrine concentration in plasma were transiently increased. Neither sulfoconjugated nor glucuroconjugated catecholamines were significantly changed. Conjugated catecholamines were measured in 10 volunteers before and at the nadir of insulin-induced hypoglycemia. As expected, plasma levels of norepinephrine and epinephrine were drastically increased. Plasma levels of sulfoconjugates were decreased and glucuroconjugates increased; these were narrow but statistically significant variations. Data reported in the present article do not support a major role for the activity of the sympathetic system in fixing the level of conjugated catecholamines in human plasma. This is a negative, but nonetheless important, observation. In human subjects, currently available information suggests an important role for the intestinal wall and renal function in determining the level of circulating sulfoconjugates.

Blood Glucose↗
PubMed1989

[Free and sulfoconjugated plasma catecholamines in premature infants and mature newborn infants after birth].

Sulfate conjugation represents a major pathway for the inactivation of free catecholamines. We investigated the ability of newborns to protect the body against an overflow of free catecholamines by sulfoconjugation. No difference of free catecholamines in the umbilical artery was found in preterm and term newborns. Furthermore, preterm and term newborns were able to form sulfoconjugated catecholamines. In term newborns, but not in preterm newborns, there was a significant relationship between free catecholamines and their respective sulfoconjugated forms (p less than 0.001). In comparison to term infants sulfoconjugated dopamine and norepinephrine were significantly decreased in preterm newborns, although the placental extraction rates of these catecholamines were markedly lower in preterm infants. This favors the conclusion, that synthesis rather than increased degradation may be responsible for the low levels of sulfoconjugated catecholamines in preterm infants. Thus, preterm newborns might be less able to inactivate free catecholamines by sulfoconjugation. The clinical importance of these results concerning treatment of preterm newborns with dopamine and noradrenaline has yet to be established.

Catecholamines↗
PubMed1984

Regulation of opioid peptide synthesis and processing in adrenal chromaffin cells by catecholamines and cyclic adenosine 3':5'-monophosphate.

Primary cultures of bovine adrenal medullary chromaffin cells were used to study the regulation of opioid peptide (OP) synthesis. Chromaffin cells continuously exposed to tetrabenazine, a drug that depletes cellular catecholamine stores, increase their OP contents between 32 hr and 6 days of treatment. At no time following tetrabenazine addition were increases in opiate receptor-inactive enkephalin-containing peptides (IECPs) observed. Because IECPs may serve as precursors to OPs, these results suggest increased processing of OP precursors following treatment with catecholamine-depleting drugs in addition to an increased rate of OP precursor synthesis. The increases in cellular OP levels induced by tetrabenazine were approximately proportional to the depletion in cellular catecholamines produced by this drug. Also, the effects of tetrabenazine on chromaffin cell OP and IECP contents were mimicked by inhibitors of catecholamine biosynthesis and other agents that decreased catecholamine stores, but not by supplementing the culture medium with catecholamines or catecholamine receptor agonists. Addition of 8-bromo-cAMP or forskolin, an activator of adenylate cyclase, to chromaffin cell cultures increased both OP and IECP stores. Inhibitors of cyclic nucleotide phosphodiesterase also increase chromaffin cell OP and IECP contents, although it is unclear whether these increases result from increased cyclic nucleotide levels. Hence, both alterations in some intracellular catecholamine pool and elevations of cAMP levels may trigger increases in the synthesis and processing of OPs and IECPs in the adrenal medullary chromaffin cell.

Adrenal Medulla↗
PubMed1994

Direct observation of the effect of autoreceptors on stimulated release of catecholamines from adrenal cells.

The direct effect of alpha 2-autoreceptors was studied by measuring the effects of piperoxan, an alpha 2-autoreceptor antagonist, and clonidine, an agonist on catecholamine exocytosis, from single bovine chromaffin cells in culture. Catecholamine release was elicited by stimulation with 100 microM nicotine and was monitored electrochemically with a carbon-fiber microelectrode placed adjacent to the cell. These electrodes allowed the number of exocytotic release events to be monitored and reported as total charge for release following a specific stimulus. Repeated stimulation with 100 microM nicotine showed that total release caused by the second exposure to nicotine was 32% of the first, and release caused by the third exposure to nicotine was 80% of the second. Total release of catecholamine increased significantly after application of 20 microM piperoxan relative to a control application of balanced salt solution. Application of 20 microM piperoxan alone did not cause release. After the cells were incubated in culture medium containing 20 microM clonidine, a significant decrease in nicotine-stimulated catecholamine release was observed. These results confirm that there are autoreceptors on chromaffin cells and, when relatively high levels of catecholamine are released, the catecholamine stimulates the alpha 2-autoreceptors, which inhibits subsequent release through a negative feedback mechanism. In addition to piperoxan, the sympathomimetic drug amphetamine also increases quantal release after application of nicotine. Amphetamine increases the extracellular concentration of catecholamine, and these data appear to indicate that at least part of the pharmacology of amphetamine might involve blocking catecholamine autoreceptors.

Adrenal Medulla↗