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PubMed1998

The hypoxia-responsive transcription factor EPAS1 is essential for catecholamine homeostasis and protection against heart failure during embryonic development.

Mice lacking the hypoxia-inducible transcription factor EPAS1 die at mid-gestation. Despite normal morphological development of the circulatory system, EPAS1-deficient mice display pronounced bradycardia. In addition to the vascular endothelium, EPAS1 is expressed intensively in the organ of Zuckerkandl (OZ), the principle source of catecholamine production in mammalian embryos. EPAS1-deficient embryos contained substantially reduced catecholamine levels. Mid-gestational lethality was rescued by administration of the catecholamine precursor DOPS to pregnant females. We hypothesize that EPAS1 expressed in the OZ senses hypoxia during mid-gestational development and translates this signal into an altered pattern of gene expression, leading to increases in circulating catecholamine levels and proper cardiac function.

Animals↗
PubMed2007

Short-term fasting-induced autonomic activation and changes in catecholamine levels are not mediated by changes in leptin levels in healthy humans.

OBJECTIVE: In animal models, the adipocyte-secreted hormone leptin increases energy expenditure by increasing sympathetic outflow but its role in humans remains to be elucidated. We evaluated whether inducing hypoleptinaemia (with and without administration of leptin at replacement doses) for 3 days would influence catecholamine levels and sympathetic and parasympathetic activity in healthy humans. METHODS: We studied six normal-weight subjects in the General Clinical Research Center (GCRC) under three conditions: baseline fed state (control study) and two 72-h fasting studies (to decrease leptin levels), with administration of either placebo or replacement-dose recombinant methionyl human leptin (r-metHuLeptin) in a randomized, double-blind fashion. In each condition, 24-h urinary catecholamine levels, heart rate and heart rate variability (HRV), a standard tool for assessing cardiac autonomic modulation, were measured. RESULTS: Study parameters remained stable during the control condition and the baseline assessment of all three studies. In response to 72-h fasting, which decreased serum leptin levels by 80%, 24-h urinary norepinephrine and dopamine levels and heart rate increased while cardiac vagal modulation decreased (all P < 0.05). Replacement-dose r-metHuLeptin to keep leptin levels within the physiological range during fasting did not alter fasting-associated changes in heart rate, catecholamine levels or cardiac vagal tone. CONCLUSIONS: The findings of this controlled, interventional study indicate that changes in heart rate, catecholamine levels and cardiac vagal modulation associated with 72-h fasting are independent of regulation by leptin. Thus, changes in leptin levels within the physiological range do not seem to play a role in regulating autonomic function during short-term starvation in healthy humans.

Adult↗
PubMed1977

Arterial and coronary sinus catecholamines and cyclic-AMP during dynamic supine exercise in patients with chest pain.

Arterial and coronary sinus catecholamine concentrations were measured during dynamic exercise in patients to assess the sympathetic response. Arterial concentrations increased from 1.77 nmol/1 (SEM = 0.53, n = 7) (control) to 2.95 nmol/1 (SEM = 0.65, n = 7) during exercise (0.05 greater than P greater than 0.01) and coronary sinus concentrations from 2.78 nmol/1 (SEM = 0.53, n = 7) (control) to 4.43 nmol/1 (SEM = 0.71, n = 7) (0.05 greater than P greater than 0.01). Resting, and exercise, arterial-coronary sinus differences in catecholamine concentrations were not statistically significant. In some patients, higher catecholamine concentrations occurred post-exercise than during exercise. The coronary sinus-arterial difference in catecholamine concentration during exercise was greatest in the one patient who developed angina pectoris. Cyclic-AMP concentrations were also measured, but these did not change significantly, consistent with the predominantly noradrenaline response to exercise.

Adult↗
PubMed1977

Segmental epidural analgesia and urinary excretion of catecholamines during labour.

Urinary excretion of catecholamines was determined separately during the first stage of labour and during the period from the beginning of the second stage until 1/2 h after delivery in 16 healthy mothers, whose labours were induced at term. Seven mothers were given segmental epidural analgesia, at the height of TH10-12, to achieve complete pain relief during the first stages of labour. The remaining parturients served as controls. During the first stage of labour the urinary excretion rate of catecholamines was at the normal nongravid rest level in both groups. During the second stage, and 1/2 h after the delivery, the amount of urinary catecholamines increased significantly in both groups. The latter values corresponded to the amounts of catecholamines excreted during heavy physicial work.

Adult↗
PubMed1991

Hemodynamic and catecholamine responses to laryngoscopy with vs. without endotracheal intubation.

To study the relationship between the intensity of the stimulus exerted against the base of the tongue during direct laryngoscopy and the magnitude of associated hemodynamic and catecholamine responses, a study was conducted in 40 ASA I or II patients. Laryngoscopy lasting 40 s was performed with a size 3 Macintosh blade connected to a force-displacement transducer. The intensity of the stimulus exerted during laryngoscopy is expressed by the product of its average force (N) and duration (s) and given as impulse in Ns. Highly significant relationships were found between the impulse during laryngoscopy and the maximal hemodynamic and catecholamine responses. Also, when laryngoscopy was followed by orotracheal intubation, significant relationships were found with steeper slopes of the regression lines for systolic blood pressure, heart rate and plasma epinephrine concentrations. A more rapid regression of hemodynamic data was seen in intubated patients, whereas their plasma catecholamine concentrations regressed more slowly. The mechanisms of the responses to laryngoscopy and orotracheal intubation are proposed to be by somato-visceral reflexes. Stimulation of proprioceptors at the base of the tongue during laryngoscopy induces impulse-dependent increases of systemic blood pressure, heart rate and plasma catecholamine concentrations. Subsequent orotracheal intubation recruits additional receptors that elicit augmented hemodynamic and epinephrine responses as well as some vagal inhibition of the heart.

Adult↗
PubMed2005

Dopamine or norepinephrine infusion during thoracic epidural anesthesia? Differences in hemodynamic effects and plasma catecholamine levels.

BACKGROUND: During thoracic epidural anesthesia, an intravenous dopamine infusion augments the systemic pressure response and modifies plasma catecholamine levels. If such an altered response occurs when norepinephrine is infused is not clear. Therefore, dopamine and norepinephrine induced circulatory and catecholamine responses were studied before and during thoracic epidural anesthesia. METHODS: Nine chloralose-anesthetized dogs were equipped with thoracic epidural catheters. Dopamine (5, 10, and 20 microg kg(-1) min(-1)), and norepinephrine (0.1, 0.25, and 0.5 microg kg(-1) min(-1)) were infused before and during epidural anesthesia, while cardiovascular performance and plasma catecholamine changes were studied. RESULTS: Thoracic epidural anesthesia decreased arterial pressure, and cardiac contractility. The systemic pressure response induced by dopamine was augmented during epidural anesthesia. Norepinephrine did not increase arterial pressure and myocardial contractility as markedly as dopamine, and cardiac output was not altered. Thoracic epidural anesthesia attenuated the plasma norepinephrine level. Plasma dopamine levels were augmented by the dopamine infusion during epidural anesthesia, while plasma norepinephrine levels were attenuated. In contrast, norepinephrine augmented the plasma norepinephrine levels during epidural anesthesia. In general, plasma norepinephrine levels were three to six times higher during a norepinephrine infusion compared to a dopamine infusion. CONCLUSION: The cardiovascular response to a graded dopamine infusion is augmented during thoracic epidural anesthesia, while norepinephrine-induced effects are unaltered. The modified plasma catecholamine levels may contribute to the hemodynamic differences between dopamine and norepinephrine infusions during thoracic epidural anesthesia.

Anesthesia, Epidural↗
PubMed1988

The effect of catecholamines and adenosine on the induction of morphological alterations and depigmentation of newt iris epithelial cells in vitro.

Catecholamines and adenosine have a stimulating effect on the process of dedifferentiation of cultured iris epithelial cells (IECs) from the adult newt Notophthalmus viridescens. Micromolar concentrations of adrenergic ligands such as isoproterenol, norepinephrine, and epinephrine induced marked morphological alterations culminating in the stellate configuration and depigmentation of IECs. Dopamine at 100 microM or higher induced the morphological response, while serotonin was ineffective. The morphological change was transient, requiring 80-90 min for maximum induction, and only a fraction of the cells was responsive. The response was blocked by beta-adrenergic antagonists, such as propranolol and alprenolol, but not by alpha-adrenergic blockers. Adenosine at 10 microM, or higher, also induced morphological alterations of IECs. The effect of adenosine was partially blocked by various adenosine receptor antagonists. The effect of isoproterenol and norepinephrine on the induction of morphological alterations was potentiated by adenosine. The release of melanosomes from IECs was increased in the presence of catecholamines and adenosine. Catecholamines and adenosine at 10 microM increased the intracellular levels of cAMP of dedifferentiating dorsal irides. The increase in cAMP levels induced by isoproterenol was inhibited by propranolol and the adenosine receptor antagonist 5'-deoxy-5'-methyl thioadenosine (MTA) partially blocked the effect of adenosine. Our results suggest that adrenergic hormones may be coupled to a beta-adrenergic adenylate cyclase system. The presence of an adenosine receptor is also suggested by the results. Our data strongly support previous work in which cAMP and substances related to it induced morphological alterations and depigmentation of IECs. It is proposed that catecholamines and adenosine may participate in the regulation of dedifferentiation during the transdifferentiation of IECs into lens cells.

Adenosine↗
PubMedDate not supplied

Stress, dopaminergic blockade and median eminence-neurointermediate lobe catecholamine depletion: effects on hypothalamic, pituitary and plasma immunoreactive beta-endorphin.

We have compared immunoreactive beta-endorphin (ir-beta EP) levels in plasma, hypothalamus, anterior pituitary and neurointermediate lobe of adult female Sprague-Dawley rats, in studies in which levels of catecholamines were manipulated. Whole-brain catecholamines were manipulated by intraperitoneal haloperidol and/or bromocriptine; median eminence and neurointermediate lobe catecholamines were manipulated specifically and differentially by intravenous 6-hydroxydopamine (6-OHDA), with and without pretreatment with intraperitoneal desipramine; changes in amine neurons were assessed by fluorescence histochemistry. Haloperidol and 6-OHDA administration produced a selective reduction of neurointermediate lobe ir-beta EP, to levels equivalent to those seen with prolonged stress; the haloperidol effect was blocked by bromocriptine and the 6-OHDA effect by desipramine. Specific depletion of catecholamine nerve terminals in the median eminence and the neurointermediate lobe was associated with elevated plasma ir-beta EP, with no changes in pituitary or hypothalamic levels. These studies confirm and extend previous reports documenting that ir-beta EP levels in different tissues are modulated by different neural stimuli.

Animals↗
PubMed1988

Modulation of adrenal catecholamine release by DA2 dopamine receptors in the anaesthetized dog.

1. The effects of DA2 agonist, quinpirole (50 micrograms/kg, i.v.) and a DA2 antagonist, domperidone (50 micrograms/kg, i.v.) on the release of adrenal catecholamines were evaluated in the anaesthetized and vagotomized dog. 2. Stimulations (5 V pulses of 2 ms duration for 3 min) of the splanchnic nerve at frequencies of 1, 3 and 5 Hz were applied randomly before and after injection of the drug. 3. The results show that quinpirole reduces significantly the release of adrenaline at 1 and 3 Hz but not at 5 Hz, while the release of noradrenaline is reduced at 1 Hz but not at 3 and 5 Hz. Inversely, domperidone potentiates significantly the release of both catecholamines at 3 and 5 Hz, but not at 1 Hz. 4. There was no change in basal release of adrenal catecholamines, adrenal blood flow or heart rate after both drug treatments. 5. The mean arterial pressure was not affected by domperidone treatment but there was a significant reduction in basal mean arterial pressure after the injection of quinpirole. 6. There was no change in any of these parameters during electrical stimulation. 7. Therefore, these results strongly suggest that DA2 dopamine receptors are present at the level of the adrenal medulla and that their activation could mediate an inhibitory modulation on the adrenal catecholamines release within a certain range of electrical stimulation.

Adrenal Glands↗
PubMed1992

Enhancement by endothelin-1 of the release of catecholamines from the canine adrenal gland in response to splanchnic nerve stimulation.

1. The effect of endothelin-1 on the release of adrenal catecholamines was examined in anaesthetized dogs. 2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz was applied before and after the intravenous injection of endothelin-1. 3. Endothelin-1 (0.1 and 0.3 micrograms/kg) significantly enhanced the release of adrenal catecholamines induced by 3 Hz SNS, but did not affect basal release and the release of adrenal catecholamines induced by 1 Hz SNS. 4. Endothelin-1 produced a slight and short-lasting fall in arterial blood pressure and decreases in adrenal and renal blood flow rates. 5. These results indicate that endothelin-1 enhances the release of adrenal catecholamines from the canine adrenal gland in response to relatively high frequency SNS.

Adrenal Glands↗
PubMed1987

Catecholamine-induced cardiopathy accompanied with pheochromocytoma.

Catecholamine-induced cardiopathy accompanied with pheochromocytoma in a 28-year-old female including two other cases are reported and the relationship between pheochromocytoma and cardiac change was also discussed. In the first case, catecholamine in the tumor tissue showed extremely high values; 94.22 micrograms/g of adrenaline and 6,332.42 micrograms/g of noradrenaline. Histologically, myocardial degeneration and inflammatory cell infiltration between myocardial fibers were noted. In the second case, hypertrophied heart showed focal degeneration of myocardial fibers with a few inflammatory cells in the stroma. The third case showed increase of heart weight, but neither myocardial degeneration nor inflammatory infiltration was noted except for moderate myocardial hypertrophy. Although the cause of difference in degree of myocardial changes is not yet clear, it may be attributed to the blood catecholamine level and/or duration of disease and/or area examined. A relative hypoxia theory is accepted for the mechanism of catecholamine-induced cardiopathy. This theory is supported by more severe lesions being noted near to the cardiac apex corresponding to peripheral coronary circulation.

Adrenal Gland Neoplasms↗
PubMed2000

Effects of hypoxia and dithionite on catecholamine release from isolated type I cells of the rat carotid body.

1. Amperometric recordings were conducted to investigate the ability of hypoxia and anoxia to evoke quantal catecholamine secretion from isolated type I cells of the rat carotid body. 2. Hypoxia (PO2 8-14 mmHg) consistently failed to evoke catecholamine secretion from type I cells, when cells were perfused either at room temperature (21-24 C) or at 35-37 C, and regardless of whether Hepes- or HCO3-/CO2-buffered solutions were used. 3. Elevating extracellular [K+] caused concentration-dependent secretion from individual type I cells, with a threshold concentration of approximately 25 mM. In the presence of this level of extracellular K+, hypoxia (PO2 8-14 mmHg) caused a marked enhancement of secretion which was fully blocked by 200 microM Cd2+, a non-specific blocker of voltage-gated Ca2+ channels. 4. Anoxia (N2-equilibrated solution containing 0.5 mM dithionite) evoked exocytosis from type I cells when extracellular [K+] was 5 mM. This secretion was completely inhibited by removal of extracellular Ca2+, but was not significantly affected by Cd2+ (200 microM), Ni2+ (2 mM), Zn2+ (1 mM) or nifedipine (2 microM). Secretion was also observed when 0.5 mM dithionite was added to air-equilibrated solutions. 5. Anoxia also evoked secretion from chemoreceptive phaeochromocytoma (PC12) cells, which was wholly Ca2+ dependent, but unaffected by Cd2+ (200 microM). 6. Our results suggest that hypoxia can evoke catecholamine secretion from isolated type I cells, but only in the presence of elevated extracellular [K+]. This may be due to the cells being relatively hyperpolarized following dissociation. In addition, we have shown that dithionite evokes catecholamine release regardless of PO2 levels, and this release is due mainly to an artefactual Ca2+ influx pathway activated in the presence of dithionite.

Animals↗
PubMed1981

Phosphorylation of adrenal medulla cell proteins in conjunction with stimulation of catecholamine secretion.

Enhanced phosphorylation of two specific protein bands accompanied catecholamine secretion from cultured bovine adrenal medulla cells stimulated by different secretagogues. Cells preincubated with 32Pi were treated with nicotine, veratridine, Ionomycin, or barium. Each of these secretagogues stimulated the phosphorylation of two protein bands with apparent molecular weights of 60,000 and 95,000. Phosphorylation of the 60,000 M. W. protein band was two- to threefold higher than that of the 95,000 M. W. band on stimulation with nicotine, veratridine, or barium, but Ionomycin stimulated phosphorylation of each protein band to the same extent. In general, the increase in phosphorylation was most rapid during the first minute of stimulation and occurred prior to detectable secretion. Phosphorylation reached a relatively constant level within 5 min after onset of stimulation at a time when catecholamine release was still proceeding at a rapid rate. Nicotine-stimulated phosphorylation and catecholamine secretion were calcium-dependent and blocked by d-tubocurarine, whereas tetrodotoxin inhibited veratridine-stimulated secretion and phosphorylation. We conclude that catecholamine secretion and protein phosphorylation occur under similar conditions and that Ca2+-dependent incorporation of phosphate into specific proteins may be a link in stimulus-secretion coupling.

Adrenal Medulla↗
PubMed1982

Relationship between Ca2+ uptake and catecholamine secretion in primary dissociated cultures of adrenal medulla.

Carbachol or elevated K+ stimulated 45Ca2+ uptake into chromaffin cells two- to fourfold. The uptake was stimulated by cholinergic drugs with nicotinic activity, but not by those with only muscarinic activity. Ca2+ uptake and catecholamine secretion induced by the mixed nicotinic-muscarinic agonist carbachol were inhibited by the nicotinic antagonist mecamylamine, but not by the muscarinic antagonist atropine. Significant Ca2+ uptake occurred within 15 s of stimulation by carbachol or elevated K+ at a time before catecholamine secretion was readily detected. At later times the time course of secretion induced by carbachol or elevated K+ was similar to that of Ca2+ uptake. There was a close correlation between Ca2+ uptake and catecholamine secretion at various concentrations of Ca2+. The concentration dependencies for inhibition of both processes by Mg2+ or Cd2+ were similar. Ca2+ uptake saturated with increasing Ca2+ concentrations, with an apparent Km for both carbachol-induced and elevated K+-induced Ca2+ uptake of approximately 2 mM. The Ca2+ dependency, however, was different for the two stimuli. The studies provide strong support for the notion that Ca2+ entry and a presumed increase in cytosolic Ca2+ concentration respectively initiates and maintains secretion. They also provide evidence for the existence of saturable, intracellular, Ca2+-dependent processes associated with catecholamine secretion. Ca2+ entry may, in addition, enhance nicotinic receptor desensitization and may cause inactivation of voltage-sensitive Ca2+ channels.

Adrenal Medulla↗
PubMed1983

Catecholamine secretion by chemically skinned cultured chromaffin cells.

The secretory system of intact chromaffin cells is not accessible to direct chemical manipulation because of the selective permeability of the plasmalemma. We have devised a simple procedure for chemically "skinning" (permeabilizing) cultured adrenal medullary chromaffin cells by brief exposure to the detergent saponin. This procedure disrupts the continuity of the plasmalemma, thus allowing us to bypass those aspects of the secretory process controlled by the cell membrane and giving direct access to exogenous substances to the cellular secretory machinery. We report here that the skinned cells retain a fully competent secretory mechanism dependent only on exogenous calcium and MgATP. Saponin treatment had no significant effect on the total catecholamine content of the cells. Secretion could be initiated by either MgATP or calcium as long as the other was present in the medium. Catecholamine and dopamine-beta-hydroxylase release by the skinned cells was dependent on the calcium concentration of the medium. The ratio of secreted catecholamine and enzyme was similar to that of the cells, indicating that secretion occurred by an exocytotic mechanism. About half the total cellular content of the cytoplasmic enzyme lactic dehydrogenase was released during the permeabilization process and subsequent incubations, indicating plasmalemma permeability to molecules as large as protein. Calcium-induced secretion was unaffected by several drugs known to affect catecholamines and granule function. Saponin treatment of chromaffin cells in culture appears to be a simple means for allowing access to exogenous substances to the cells' secretory machinery. Therefore, it offers the opportunity to use chemical treatments, and perhaps specific antibodies to cellular components, to determine the role of these elements in the secretory process. These techniques should also be applicable to other cells known to secrete by an exocytotic mechanism.

Adenosine Triphosphate↗
PubMed1984

The relationship between arachidonic acid release and catecholamine secretion from cultured bovine adrenal chromaffin cells.

Increased arachidonic acid release occurred during activation of catecholamine secretion from cultured bovine adrenal medullary chromaffin cells. The nicotinic agonist 1,1-dimethyl-4- phenylpiperazinium (DMPP) caused an increased release of preincubated [3H]arachidonic acid over a time course which corresponded to the stimulation of catecholamine secretion. Like catecholamine secretion, the DMPP-induced [3H]arachidonic acid release was calcium-dependent and was blocked by the nicotinic antagonist mecamylamine. Depolarization by elevated K+, which induced catecholamine secretion, also stimulated arachidonic acid release. Because arachidonic acid release from cells probably results from phospholipase A2 activity, our findings indicate that phospholipase A2 may be activated in chromaffin cells during secretion.

Adrenal Medulla↗
PubMed1985

Membrane potential and catecholamine secretion by bovine adrenal chromaffin cells: use of tetraphenylphosphonium distribution and carbocyanine dye fluorescence.

Changes in plasma membrane potential of isolated bovine adrenal chromaffin cells were measured independently by two chemical probe methods and related to corresponding effects on catecholamine secretion. The lipophilic cation tetraphenylphosphonium (TPP+) and the carbocyanine dye 3,3'-dipropylthiadicarbocyanine [DiS-C3-(5)] were used. The necessity of evaluating the subcellular distribution of TPP+ among cytoplasmic, mitochondrial, secretory granule, and bound compartments was demonstrated and the resting plasma membrane potential determined to be -55 mV. The relationship between membrane potential and catecholamine secretion was determined in response to variations in extracellular K+ and to the presence of several secretagogues including cholinergic receptor ligands, veratridine, and ionophores for Na+ and K+. The dependence of potential on K+ concentration fit the Goldman constant field equation with a Na/K permeability ratio of 0.1. The dependence of both K+- and veratridine-evoked catecholamine secretion on membrane potential exhibited a potential threshold of about -40 mV before a significant rise in secretion occurred. This is likely related to the threshold for opening of voltage-sensitive Ca2+ channels. Acetylcholine and nicotine evoked a large secretory response without a sufficiently sustained depolarization to be detectable by the relatively slow potential sensitive chemical probes. Decamethonium induced a detectable depolarization of the chromaffin cells. Veratridine and gramicidin evoked both membrane depolarization and catecholamine release. By contrast the K ionophore valinomycin evoked significant levels of secretion without any depolarization. This is consistent with its utilization of an intracellular source of Ca2+ and the independence of its measured secretory response on extracellular Ca2+.

Acetylcholine↗
PubMed1987

Calcium dependence of muscarinic receptor-mediated catecholamine secretion from the perfused rat adrenal medulla.

It had previously been thought that muscarinic cholinergic receptors utilize an influx of extracellular calcium for activation of adrenomedullary catecholamine secretion. However, it has recently been demonstrated that muscarinic receptors on isolated adrenal chromaffin cells can elevate cytosolic free calcium levels in a manner independent of extracellular calcium, presumably by mobilizing intracellular calcium stores. We now demonstrate that muscarinic receptor-mediated catecholamine secretion from perfused rat adrenal glands can occur under conditions of extracellular calcium deprivation that are sufficient to block both nicotine- and electrically stimulated release. Three independent conditions of extracellular calcium deprivation were used: nominally calcium-free perfusion solution (no calcium added), EGTA-containing calcium-free perfusion solution, and perfusion solution containing the calcium channel blocker verapamil. Secretion was evoked from the perfused glands by either transmural electrical stimulation or injection of nicotine or muscarine into the perfusion stream. Each condition of calcium deprivation was able to block nicotine- and electrically stimulated catecholamine release in an interval that left muscarine-evoked release largely unaffected. The above results demonstrate that muscarine-evoked catecholamine secretion from perfused rat adrenal glands can occur in the absence of extracellular calcium, presumably by mobilization of intracellular calcium. The latter may be due to muscarinic receptor-mediated generation of inositol trisphosphate.

Adrenal Medulla↗