Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CATECHOLAMINES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 577 records · Page 32Linked to original sources
PubMed1982

Non-neurogenic mechanism for reserpine-induced release of catecholamines from the adrenal medulla of neonatal rats: possible modulation by opiate receptors.

Neonatal rats do not have functional splanchnic nerve connections to the adrenal medulla until approximately one week of postnatal age, yet they are able to respond to some drugs or stresses by releasing adrenal catecholamines. Reserpine (5 mg/kg s.c.) resulted in significant loss (20-40%) of neonatal catecholamines within 4 h; unlike the acute effects of reserpine in the adult, depletion was not prevented by pretreatment with a nicotinic blocking agent, demonstrating that the effect in the neonate is non-neurogenic. Depletion did not result simply from inhibition of catecholamine storage by reserpine, but rather, the non-neurogenic depletion represented net movement of the amines from the storage granules into the extracellular space, as evaluated by the subcellular distribution of catecholamines. These results suggest that the non-neurogenic mechanism represents release of catecholamines. The immature response mechanism disappeared by 11 days of age and was replaced by a completely neurogenic release, demonstrating that the special mechanism is lost within several days of the onset of functional innervation of the adrenal. Experiments also were carried out to test whether endogenous opioids and/or opiate receptors are involved in the non-neurogenic mechanism. Naloxone (5 mg/kg s.c.) potentiated the depletion of catecholamines by reserpine, while methadone (2.5 mg/kg s.c.) inhibited the non-neurogenic response. In contrast, no potentiation of release by naloxone or inhibition by methadone was seen in adult rats. Thus, opiate receptors may modulate only the immature secretory mechanism.

Adrenal Medulla↗
PubMed1988

Comparison of secretion of catecholamines from the rat adrenal medulla during continuous exposure to nicotine, muscarine or excess K.

The effects of continuous exposure of chromaffin cells to nicotine, muscarine and excess potassium on the secretion of catecholamines and uptake of radiolabeled calcium were investigated in the isolated perfused adrenal gland of the rat. Perfusion with 20 microM nicotine-Krebs solution increased catecholamine secretion from a basal value of 5 ng to 273 ng in the first 5 min. The secretion declined to about 20 ng after 30 min of continuous exposure to nicotine (slow desensitization). 200 microM muscarine increased the secretion to about 150 ng within the first 5-10 min, and remained at the level of 110 ng even after continuous perfusion with muscarine for up to 40 min (no desensitization). About 700 ng of catecholamines were secreted within the first 5 min of exposure to 55 mM K, the secretion declined to about 350 ng in the next 5 min, and remained almost at this level for 120 min during continuous perfusion with excess K (partial desensitization). When the secretion of catecholamines was depressed by continuous exposure to nicotine for 30 min, introduction of 55 mM K or 200 microM muscarine (along with nicotine) still led to a large increase in the secretion of catecholamines. Omission of calcium ions from the perfusion medium containing either nicotine or 55 mM K caused a rapid decline in the secretion of catecholamines, suggesting influx of external calcium, but muscarine-induced secretion was only modestly reduced by calcium removal, suggesting mobilization of internal calcium. Addition of EGTA to calcium-free medium completely abolished the secretion evoked by all agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1987

Determination of catecholamines in urine (and plasma) by liquid chromatography after on-line sample pretreatment on small alumina or dihydroxyborylsilica columns.

The possibilities of the on-line pre-concentration of catecholamines on small columns packed with aluminium oxide (10 micron) or dihydroxyborylsilica (5 micron) prior to high-performance liquid chromatography (HPLC) were investigated. For both pre-concentration materials the influence of the pH of the mobile phase on the retention characteristics was studied for the catecholamines and some of their derivatives lacking the catechol and/or the amine function. The recovery of the catecholamines and the loading capacity on some pre-columns was then investigated. The compatibility of the pre-concentration system with several HPLC systems, viz., reversed-phase ion-pair, ion-exchange and reversed-phase ion-pair partition chromatography, was studied. Combined with amperometric or fluorimetric detection, the method was applied to the determination of free catecholamines in urine, using dihydroxybenzylamine or epinine as internal standards. An example of the determination of catecholamines in plasma containing 100 pg/ml of each catecholamine is also shown.

Adsorption↗
PubMed1995

Characteristics of ATP-induced catecholamine secretion from adrenal chromaffin cells of the guinea-pig.

The effect of ATP on catecholamine secretion and intracellular Ca2+ concentration ([Ca2+]i) was examined using perfused adrenal glands and dispersed chromaffin cells of the guinea-pig. The application of ATP (2 to 10 mM) for 2 min caused a dose-dependent increase in catecholamine secretion from perfused adrenal glands. ADP, but neither AMP nor adenosine, was also effective in increasing catecholamine secretion, though its potency was much less than that of ATP. 3. The ATP-induced secretory response was observed even under Na(+)-deficient conditions, but was reversibly abolished by removal of extracellular Ca2+. 4. In dispersed chromaffin cells, ATP (0.5 mM) caused increases in catecholamine secretion and [Ca2+]i, both of which were abolished after the removal of extracellular Ca2+. 5. These results indicate that ATP released from adrenal chromaffin cells together with catecholamine may exert a positive feedback influence on the following exocytotic catecholamine secretion. This effect may be accomplished by increasing the entry of extracellular Ca2+, but not by mobilizing intracellular Ca2+ stores in adrenal chromaffin cells of the guinea-pig.

Adenine Nucleotides↗
PubMed2005

Inhibition of the RhoA/Rho kinase system attenuates catecholamine biosynthesis in PC 12 rat pheochromocytoma cells.

The small GTPase, RhoA, and its downstream effecter Rho-kinase (ROK) are reported to be involved in various cellular functions, such as myosin light chain phosphorylation during smooth muscle contraction and exocytosis. Indeed, growing evidence suggests that the RhoA/Rho-kinase pathway plays an important role in regulating exocytosis in these cells. However, it is not known whether the RhoA/Rho-kinase pathway has an effect on catecholamine synthesis. Using the rat pheochromocytoma cell line, PC12, we examined the effects of either Rho-kinase inhibitor (Y27632) or RhoA inhibitor (C3 toxin) on nicotine-induced catecholamine biosynthesis. We show that nicotine (10 microM) induces a significant, though transient, increase in RhoA activation in these cells. Treatment with either Y27632 (1 microM) or C3 toxin (10 microg/ml) significantly inhibited the nicotine-induced increase of tyrosine hydroxylase (TH) mRNA and the corresponding enzyme activity. TH catalyzes the rate-limiting step in the biosynthesis of catecholamine. Y27632 significantly inhibited nicotine-induced phosphorylation of TH at Ser40 as well as Ser19, which are known to be phosphorylated by Ca(2+)/calmodulin kinase II. Furthermore, Y27632 (10 microM) as well as C3 toxin (10 microg/ml) significantly inhibited the nicotine-induced increase of TH at the protein level. Thus, we propose that activation of RhoA, and its downstream effecter Rho-kinase, is a prerequisite for catecholamine biosynthesis in PC12 cells. At the concentrations used in our experiments, Y27632 does not affect cAMP/PKA activity or PKC activity, indicating that the inhibitory effect of Y27632 can be attributed to the inhibition of Rho-kinase activity as observed in chromaffin cells. In contrast, neither Y27632 (10 microM) nor C3 toxin (10 microg/ml) significantly altered catecholamine secretion in PC12 cells. In conclusion, we have demonstrated that inhibition of the Rho/Rho-kinase pathway in chromaffin cells lowers TH activity, probably through CaMKII inhibition. By contrast, neither Y27632 nor C3 toxin affect the secretion of catecholamine.

Amides↗
PubMed2004

Developmental regulation of catecholamine levels during sea urchin embryo morphogenesis.

Results of a number of pharmacological studies suggest that catecholamines play a regulatory role in cleavage, morphogenesis and cell differentiation during early animal embryonic development. Few studies, however, have actually assayed for levels of catecholamines in these early embryos by methods that are both sensitive and specific. In this investigation the catecholamines dopamine, norepinephrine and epinephrine and their precursor, dopa and metabolites were determined in eight different embryonic stages of the sea urchin, Lytechinus pictus from hatched blastula to late pluteus larva, using high performance liquid chromatography with electrochemical detection. Levels of each of the catecholamines exhibited unique developmental profiles and are consistent with a role for epinephrine in blastula and early gastrula embryos and for norepinephrine in gastrulation. Changes in levels of catecholamine precursor and metabolites suggest a changing pattern of synthetic and metabolic enzyme activity, which can, for the most part, explain the fluctuations in catecholamine levels during development from blastula to the pluteus larva stage.

Animals↗
PubMed2004

The effects of candesartan and ramipril on adrenal catecholamine release in anaesthetized dogs.

We have investigated the effects of the angiotensin II type 1 receptor antagonist candesartan, and the angiotensin II converting enzyme inhibitor ramipril, on catecholamine release from the anaesthetized dog's adrenal gland. These drugs were given systemically in low and high doses. The gland was stimulated electrically (0.5-12 Hz) and by angiotensin II infusion (40 ng/kg/min). Electrical stimulation resulted in frequency-dependent increases in catecholamine release. Candesartan (0.8, 4.0 mg/kg) and ramipril (0.125, 0.625 mg/kg) increased basal catecholamine release along with decreases in blood pressure. Both drugs diminished direct nerve stimulation-induced catecholamine release. When both drugs were combined, their inhibitory effect was slightly enhanced. Candesartan blocked catecholamine release induced by angiotensin II. Ramipril was not tested in this respect. The percentage of noradrenaline released during electrical stimulation of the gland remained constant and ranged from 14% to 22%. Both drugs appear to act by blocking local modulation of catecholamine release by the chromaffin cells.

Adrenal Glands↗
PubMed2004

Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity.

The mechanisms underlying the onset of obesity are complex and not completely understood. An imbalance of autonomic nervous system has been proposed to be a major cause of great fat deposits accumulation in hypothalamic obesity models. In this work we therefore investigated the adrenal chromaffin cells in monosodium glutamate (MSG)-treated obese female mice. Newborn mice were injected daily with MSG (4 mg/g body weight) or saline (controls) during the first five days of life and studied at 90 days of age. The adrenal catecholamine content was 56.0% lower in the obese group when compared to lean controls (P < 0.0001). Using isolated adrenal medulla we observed no difference in basal catecholamine secretion percentile between obese and lean animals. However, the percentile of catecholamine secretion stimulated by high K+ concentration was lower in the obese group. There was a decrease in the tyrosine hydroxylase enzyme expression (57.3%, P < 0.004) in adrenal glands of obese mice. Interestingly, the expression of dopamine beta-hydroxylase was also reduced (47.0%, P < 0.005). Phenylethanolamine N-methyltransferase expression was not affected. Our results show that in the MSG model, obesity status is associated with a defective adrenal chromaffin cell function. We conclude that in MSG obesity the low total catecholamine content is directly related to a decrease of key catecholamine-synthesizing enzymes, which by its turn may lead to a defective catecholamine secretion.

Adrenal Medulla↗
PubMed2005

Effect of preventive and regressive isosorbide 5-mononitrate treatment on catecholamine levels in plasma, platelets, adrenals, left ventricle and aorta in cyclosporin A-induced hypertensive rats.

Increased vascular reactivity associated with cyclosporin A (CsA)-induced arterial hypertension might result from increased vasoconstriction and/or decreased vasodilatation. The administration of organic NO donors could have beneficial effects by the NO-cGMP reposition, but there is the risk of sympathetic nervous system worsening by neuro-hormonal counter-regulation. We evaluate the effect of preventive and regressive (curative) isosorbide 5-mononitrate (Is-5-Mn) treatment on blood pressures and on plasma, platelets, adrenals, left ventricle and aorta norepinephrine (NE) and epinephrine (E) contents, assessed by HPLC, in CsA-induced hypertensive rats. Five rat groups were tested: control (orange juice), CsA (5 mg/kg/day) and Is-5-Mn (150 mg/kg/day, bid) groups were treated for 7 weeks; preventive group (Is-5-Mn+CsA): Is-5-Mn during 2 weeks plus 7 weeks of Is-5-Mn+CsA; regressive group (CsA+Is-5-Mn): CsA during 7 weeks plus 5 weeks of CsA+Is-5-Mn. The increased BP in the CsA group was prevented, but was not reverted, by concomitant Is-5-Mn treatment. In the CsA-treated rats, there was a noticeable decrease in left ventricle NE and E contents and aorta NE levels and a moderate increase in circulating catecholamines, without significant effect in the adrenals values. When Is-5-Mn was preventively used, the CsA-induced effect on left ventricle and aorta was prevented. Concomitantly, however, the plasma-platelet catecholamine balance was disrupted, accumulating NE in plasma, whereas E increased in aorta, mimic the single Is-5-Mn-treated group. In opposition, in the group used as regressive Is-5-Mn therapy, the adrenals contents were higher compared with the CsA-group and, simultaneously, the CsA-evoked effects on circulating, left ventricle and aorta catecholamines were not reverted. In conclusion, regressive Is-5-Mn therapy was unable to attenuate CsA-induced catecholamine changes and BP values even worsened. On the contrary, preventive Is-5-Mn treatment prevented the catecholamine changes on left ventricle and aorta, but increased plasma NE and aorta E accumulation. Even though with those effects, hypertension development was totally prevented, suggesting that peripheral SNS per se cannot fully explain CsA-induced hypertension. Furthermore, Is-5-Mn might produce beneficial effects only if preventively employed but, considering the changes on peripheral catecholamine contents, a judicious evaluation of the nitrate therapy impact is recommended in order to avoid further deleterious effects.

Adrenal Glands↗
PubMed2006

Midkine is a potent regulator of the catecholamine biosynthesis pathway in mouse aorta.

To discover regulatory pathways dependent on midkine (Mk the gene, MK the protein) signaling, we compared the transcriptional profiles of aortae obtained from Mk -/- and wild type (WT, +/+) mice; the comparison demonstrated an extraordinary high level expression of tyrosine hydroxylase (12-fold), the rate-limiting enzyme in catecholamine biosynthesis, DOPA decarboxylase (73-fold), and dopamine beta-hydroxylase (75-fold) in aortae of Mk -/- mice compared with aortae of WT (+/+) mice. Phenylethanolamine-N-methyltransferase, the enzyme catalyzing the conversion of norepinephrine into epinephrine, was not detected in either Mk -/- and WT (+/+) mouse aorta. The protein levels of tyrosine hydroxylase, DOPA decarboxylase and dopamine beta-hydroxylase confirmed the analysis of the transcriptional profiles. Surprisingly, MK failed to regulate the enzymes of the catecholamine biosynthesis pathway in 10 other tissues studied. Furthermore, the expression levels of the enzymes of catecholamine biosynthesis in aortae of Mk -/- mice were effectively the same as those in aortae of Pleiotrophin (Ptn the gene, PTN the protein) genetically deficient (Ptn -/-) mice when compared with WT (+/+) mice. The remarkable increases in levels of expression of tyrosine hydroxylase, DOPA decarboxylase and dopamine beta-hydroxylase suggest that MK together with PTN are very important regulators of the catecholamine pathway in mouse aorta and may critically regulate catecholamine biosynthesis and function in inflammatory and the other pathological conditions in which Mk or Ptn are upregulated. The data also establish that norepinephrine is effectively the only catecholamine synthesized in mouse aorta.

Animals↗
PubMed2005

Post-resuscitation plasma catecholamines after prolonged arrest in a swine model.

OBJECTIVE: A dramatic increase in plasma catecholamines has been demonstrated consistently following cardiac arrest and during CPR. The time course of this initial catecholamine surge after successful resuscitation has not been well studied. The purpose of this study was to measure plasma catecholamines after successful resuscitation and to determine their relationship to post-resuscitation hemodynamics. METHODS: VF cardiac arrest was induced in eight anesthetized and instrumented swine. After 5 min of VF, conventional CPR was initiated followed 2 min later by transthoracic defibrillation. Restoration of spontaneous circulation (ROSC) was achieved in six animals. Following resuscitation, hemodynamic variables and plasma catecholamines were measured at intervals. RESULTS: Myocardial contractility (peak systolic dP/dt), stoke volume, left ventricular stroke work (LVSW), and mean arterial pressure (MAP) were significantly decreased from pre-arrest values within 15 min of ROSC and remained depressed during 60 min of observation. Systemic vascular resistance (SVR) was significantly increased within 15 min and remained elevated. Significant negative correlations were observed between SVR and plasma epinephrine (adrenaline) (r=-0.72, p<0.001) and norepinephrine (noradrenaline) (r=-0.76, p<0.001). Significant negative correlations were also observed between MAP and these catecholamines. A negative correlation was also observed between norepinephrine and LVSW (r=-0.50, p=0.039). Catecholamine levels were not related to other indices of cardiac function. CONCLUSIONS: A post-resuscitation adrenergic state is driven by a decline in MAP and PVR. Although seemingly compensatory, it may also contribute to the observed decline in cardiac function.

Animals↗
PubMed2001

Characterization of ginseng saponin ginsenoside-Rg(3) inhibition of catecholamine secretion in bovine adrenal chromaffin cells.

Since ginsenoside-Rg(3), one of the panaxadiol saponins isolated from the ginseng root, significantly inhibited the secretion of catecholamines from bovine adrenal chromaffin cells stimulated by acetylcholine (ACh), the properties of ginsenoside-Rg(3) inhibition were investigated. Although ginsenoside-Rg(3) inhibited the secretion evoked by ACh in a concentration-dependent manner, it affected the secretion stimulated by high K(+) or veratridine, an activator of the voltage-sensitive Ca(2+) or Na(+) channels, only slightly. The ACh-induced Na(+) and Ca(2+) influxes into the cells were also reduced by ginsenoside-Rg(3). The inhibitory effect of this saponin on the secretion of catecholamines was not altered by increasing the external concentration of ACh or Ca(2+). The ACh-evoked secretion of catecholamines was completely restored in cells that were preincubated with 10 microM ginsenoside-Rg(3) and then incubated without the saponin, whereas secretion was not completely restored in cells that were preincubated with 30 microM of this compound. Above 30 microM ginsenoside-Rg(3) increased the fluorescence anisotropy of diphenylhexatriene in the cells. Furthermore, the inhibitory effect of ginsenoside-Rg(3) at 30 microM on the ACh-evoked secretion of catecholamines was dependent upon the preincubation time, but this was not the case at 10 microM. These results strongly suggest that ginsenoside-Rg(3) blocks the nicotinic ACh receptor-operated cation channels, inhibits Na(+) influx through the channels, and consequently reduces both Ca(2+) influx and catecholamine secretion in bovine adrenal chromaffin cells. In addition to this action, the ginsenoside at higher concentrations modulates the fluidity of the plasma membrane, which probably contributes to the observed reduction in the secretion of catecholamines.

Acetylcholine↗
PubMed2000

Role of endogenous endothelins in catecholamine secretion in the rat adrenal gland.

We investigated the role of endogenous endothelins in catecholamine secretion in response to transmural electrical stimulation in the retrogradely perfused rat adrenal gland. (R)2-[(R)-2-[(S)-2-[[1-(hexahydro-1H-azepinyl)]carbonyl]amino-4-++ +methy l-pentanoyl]amino-3-[3-(1-methyl-1H-indoyl)]propionyl]amino-3-(2-+ ++pyridyl) propionic acid (FR139317; 0.03-3 microM), an endothelin ET(A) receptor antagonist, inhibited the electrical stimulation-induced epinephrine and norepinephrine output. Neither N-cis-2, 6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D-1- methoxycarbonyl tryptophanyl-D-norleucine (BQ-788; 0.03-3 microM), an endothelin ET(B) receptor antagonist, nor phosphoramidon (1-100 mM), an endothelin-converting enzyme inhibitor, affected the catecholamine output responses. However, the inhibition by FR139317 of the catecholamine output responses was abolished by pretreatment with phosphoramidon (100 mM) or BQ-788 (3 microM). These results indicate that activation of endothelin ET(B) receptors by endogenous endothelins inhibits the catecholamine output responses under the condition in which endothelin ET(A) receptors are blocked. Exogenous endothelin-1 (1-100 nM) did not affect the catecholamine output responses, but it inhibited the responses under treatment with phosphoramidon and FR139317. Activation of endothelin ET(A) receptors may interfere with the endothelin ET(B) receptor-mediated inhibitory action on the neuronally evoked secretion of adrenal catecholamines.

Adrenal Glands↗
PubMed2002

Characterization of functional nicotinic acetylcholine receptors involved in catecholamine release from the isolated rat adrenal gland.

We tried to characterize nicotinic acetylcholine receptors involved in the release of catecholamines from the rat adrenal gland. The isolated adrenal gland was retrogradely perfused via the adrenal vein with Krebs-Ringer solution at a flow rate of 0.5 ml/min. Endogenous catecholamines, adrenaline and noradrenaline, released into the perfusate were electrochemically measured using high-performance liquid chromatography. (-)-Nicotine (3 x 10(-6)-3 x 10(-5) M) evoked the release of catecholamines (adrenaline >> noradrenaline) in a concentration-dependent manner. The (-)-nicotine (10(-5) M)-induced release of catecholamines was effectively attenuated by mecamylamine (10(-7) and 10(-6) M) (a relatively selective antagonist of alpha3beta4 nicotinic receptors), but not influenced by alpha-bungarotoxin (3 x 10(-7) M) (an antagonist of alpha7 nicotinic receptors) and dihydro-beta-erythroidine (10(-5) M) (a relatively selective antagonist of alpha4beta2 nicotinic receptors). (+/-)-Epibatidine (3 x 10(-7) and 10(-6) M) (a non-selective nicotinic receptor agonist), (-)-cytisine (10(-5) and 10(-4) M) (an agonist of beta4 nicotinic receptors) and (+/-)-2-(3-pyridinyl)-1-azabicyclo(2.2.2)octane (RJR-2429) (10(-5) M) (a putative agonist of alpha3beta4 nicotinic receptors) effectively evoked the release of catecholamines (adrenaline >> noradrenaline), while (E)-N-methyl-4-(3-pyridinyl)-3-butene-1-amine (RJR-2403) (up to 10(-4) M) (a selective agonist of alpha4beta2 nicotinic receptors) had no effect. The efficacies of these agonists are as follows: (+/-) epibatidine >> RJR-2429>(-)-cytisine>(-)-nicotine >> RJR-2403. These results suggest that alpha3beta4 nicotinic receptors are involved in the release of catecholamines from the rat adrenal gland.

Adrenal Glands↗
PubMed1988

Improved solid-phase extraction and liquid chromatography with electrochemical detection of urinary catecholamines and 5-S-L-cysteinyl-L-dopa.

We describe a rapid, precise, accurate liquid chromatographic procedure for determining urinary catecholamines and 5-S-L-cysteinyl-L-dopa. The catecholamines (norepinephrine, epinephrine, and dopamine) and 5-S-L-cysteinyl-L-dopa are extracted from 1.0 ml of urine together with internal standards, by using a Bond-Elut strong cation-exchange (SCX) and an affinity phenylboronic acid (PBA) extraction column in series. The eluate obtained from PBA column is then chromatographed on a reversed-phase C18 column with a mobile phase containing pentane- and heptanesulfonate as ion-pair reagents. The detection is achieved with an amperometric detector set at an oxidation potential of +0.55 V. The chromatography is complete is less than 8 min for catecholamines and less than 5 min for cysteinyldopa. The method can measure less than 2 micrograms/l for catecholamines and 5 micrograms/l for cysteinyldopa. Analytical recoveries of catecholamines and cysteinyldopa added to urine pool ranged from 90-107%. Between run coefficient of variation ranged from 4.7 to 8%. None of the drugs and catecholamines metabolites tested interfered with the assay.

Catecholamines↗
PubMed2000

Effects of natriuretic peptides (ANP, BNP, CNP) on catecholamine synthesis and TH mRNA levels in PC12 cells.

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are present in adrenal chromaffin cells, and are co-secreted with catecholamines suggesting that these natriuretic peptides (NPs) may modulate functions of chromaffin cells in an autocrine and/or paracrine manner. Therefore, we investigated the effects of NPs on tyrosine hydroxylase (TH: a rate-limiting enzyme in biosynthesis of catecholamine) mRNA in rat pheochromocytoma PC12 cells. It was also determined whether the cyclic GMP/cGMP-dependent protein kinase (cGMP/PKG) pathway was involved in theses effects. Finally, we examined the effects of NPs on intracellular catecholamine content to confirm increase of catecholamine synthesis following TH mRNA induction. NPs (0.1 microM) induced significant increases of the TH mRNA (ANP= BNP> CNP). Also, the effects of NPs on TH mRNA were mimicked by 8-bromo cyclic GMP (1mM), and were blocked by KT5823 (1 microM) (inhibitor PKG) or LY83583 (1 microM) (guanylate cyclase inhibitor). Moreover, NPs were shown to induce significant increases of intracellular catecholamine contents (ANP= BNP> CNP). These findings suggest that NPs induced increases of TH mRNA through cGMP/PKG dependent mechanisms, which, in turn, resulted in stimulation of catecholamine synthesis in PC12 cells.

Animals↗
PubMed1996

The role of catecholamines in cocaine toxicity: a model for cocaine "sudden death".

Sudden death associated with cocaine abuse is preceded by a state of agitated delirium. We postulated that release of catecholamines associated with this stress enhanced toxicity from cocaine. Thus we investigated the effect of catecholamine infusion [(epinephrine (7.25 ugml-1), norepinephrine (4.4 ugml-1) and dopamine (8.0 ugml-1), infused at 6 ml h-1] on the toxicity from concomitant infusion of cocaine (1 mg-kg-1 min-1). Two groups of rats were studied in order to isolate distinct toxicity endpoints: convulsions and respiratory arrest in conscious, and, circulatory arrest in anesthetized and ventilated rats. Catecholamines were administered at either full or 1/2 strength to establish a dose response effect on cocaine toxicity. Catecholamine infusion in a dose dependent fashion provoked earlier convulsions and respiratory arrest in conscious rats and circulatory arrest in anesthetized and ventilated rats. Despite lower cocaine cumulative dose administration, rats receiving catecholamines had similar plasma cocaine concentrations at the onset of convulsions and respiratory arrest compared to those with cocaine infusion alone. The data suggest that catecholamines enhance the convulsive, respiratory and circulatory toxicity of cocaine by a pharmacokinetic interaction.

Animals↗
PubMed2000

Liver ischemia, catecholamines and preoperative condition influencing postoperative tachycardia in liver surgery.

The aim of our study was to assess the influence of intraoperative hypoxic stress -unavoidably brought about by so called Pringle maneuver - on free and conjugated catecholamines during major hepatic resection. Judging from earlier results of fatigue-experiments in rats we also wanted to check the relationship between of poor general preoperative condition and conspicuously low triglyceride serum concentrations. The study included 26 patients with primary and secondary liver tumors. The mean age was 54 years (range 27-79). Twenty-one patients had segmental liver resections, 3 had hemihepatectomies and 2 hydatid cysts were treated by cystectomy. Blood samples were taken 2 days before and throughout surgery. Catecholamine plasma values were determined by high performance liquid chromatography. Statistical comparisons were made by t-test, ANOVA and chi square test. Free plasma catecholamines increased significantly during prolonged intraoperative ischemia (Pringle time 50-125 minutes). Patients with elevated intraoperative catecholamines had a significant correlation to postoperative episodes of tachycardia, and prolonged hospital stay. On the other hand, we could also see postoperative tachycardias in patients with short Pringle times (18-49 minutes) but with decreased preoperative serum triglycerides as an indicator of chronic stress and reduced general condition. Intraoperative hypoxic stress is associated with increased catecholamine values. Elevated catecholamines may well cause postoperative sinus-tachycardias (mean 20 hours) and are strongly related to postoperative liver failure and prolonged hospital stay.

Adult↗