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PubMedDate not supplied

Role of atrial natriuretic peptide on calcium channel mechanisms involved in catecholamine release from bovine adrenal medulla.

The role of the atrial natriuretic peptide on calcium channel mechanisms involved in catecholamine release was studied in the perfused bovine adrenal medulla. The atrial natriuretic peptide (1 nM and 10 nM) did not modify the spontaneous release of catecholamines. Ten nM of atrial natriuretic peptide decreased the output of catecholamines induced by acetylcholine, KCl-depolarizing solutions and angiotensin II. It was ineffective to modify the catecholamine release when calcium channels were blocked or in the presence of calcium-free media. Moreover, the deprivation of the ion calcium in the media decreased the catecholamine release induced by KCl to a lowest level, despite the presence of atrial natriuretic peptide in the perfusate. In conclusion, atrial natriuretic peptide inhibited the induced secretion of catecholamines in the bovine adrenal medulla and interfered as a partial blocker with calcium-dependent mechanisms.

Acetylcholine↗
PubMedDate not supplied

Plasma atrial natriuretic factor and catecholamines before and during excision of pheochromocytoma.

We studied changes of atrial natriuretic factor (ANF) and catecholamines in three patients with pheochromocytoma occurring in the familial syndrome of multiple endocrine neoplasia type IIa. Previous studies have suggested a stimulating effect of catecholamines on ANF release. In pheochromocytoma, we observed normal basal ANF levels despite increased catecholamine secretion. In contrast, a rise in plasma ANF was observed when a hypertensive paroxysm occurred. Also during surgery, dissection of pheochromocytoma led to a rise in plasma ANF and catecholamines associated with an increase in blood pressure (in the 3 cases) and in pulmonary artery pressure (in 2 cases). We concluded that chronic elevation of basal catecholamines are without effect on plasma ANF but that manipulation of pheochromocytoma leads to a stimulation of ANF release, possibly mediated by either a direct effect of endogenously released catecholamines and/or an increase in atrial pressure.

Adrenal Gland Neoplasms↗
PubMed1990

Catecholamine metabolism in heart failure patients and healthy control subjects.

Parameter of catecholamine metabolism were examined in patients (Groups II to V) in chronic, stable stages of coronary heart disease (n = 45), dilated cardiomyopathy (n = 17) and healthy control subjects (Group I). Plasma and urinary catecholamine patterns, catecholamine plasma half-life and catecholamine metabolism following administration of levodopa were determined. In cases of slight (Group II, ejection fraction (EF) 54 +/- 7%) to marked left-heart damage (Group III, EF 44 +/- 5%), the findings indicate elevated catecholamine excretion and a beginning reduction of plasma clearance as the cause of excessive, circulating and renally excreted catecholamines (applies to noradrenaline, less to adrenaline). The renal 24-h dopamine elimination is already slightly reduced in these patients. In cases of severe left-heart damage, the findings are not uniform. In some cases, noradrenaline at rest and at comparable exercise levels are elevated (Group IV, EF 20 +/- 11%), in some cases they are normal (Group V, EF 16 +/- 4%). The 24-h dopamine elimination is reduced in both groups to 34-41% of normal. Noradrenaline and adrenaline elimination is normal, or reduced (Group V, adrenaline). The exercise-induced, maximum plasma noradrenaline concentrations in Group IV and V are much lower (33-40% of normal) than in the healthy control individuals and patients in Groups II and III. Oral administration of 2-4 g levodopa per day result in a 20- to 40-fold dopamine increase in patients with heart failure (Group IV) and healthy control persons (Group I) (free and conjugated plasma dopamine, as well as free urinary dopamine).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Catecholamines in myocardial ischemia. Systemic and cardiac release.

During myocardial ischemia, malignant arrhythmias and acceleration of cell damage may be induced by sympathetic overstimulation of the heart. This stimulation is due to excessive concentrations of catecholamines within the underperfused myocardium, in combination with enhanced myocyte sensitivity to adrenergic stimuli. Various mechanisms may account for local accumulation of catecholamines in the extracellular space of the ischemic but still viable myocardium. In early myocardial infarction, plasma noradrenaline and adrenaline concentrations are enhanced, reflecting increased activity of the whole sympathetic nervous system, rather than local activity in the heart. In uncomplicated infarction, these concentrations are only five times the normal levels at rest, and there are no convincing data that these mildly increased levels of plasma catecholamines directly induce a major deterioration of myocardial function during the ischemic process. Of more importance is the reflex increase in cardiac sympathetic nerve activity that is induced by pain, anxiety, and a fall in cardiac output or arterial blood pressure and that is accompanied by local exocytotic release of noradrenaline from sympathetic nerve endings of the heart. Excessive accumulation of the neurotransmitter, however, is prevented by at least three mechanisms: 1) Released noradrenaline is rapidly removed so long as neuronal catecholamine reuptake is functional. 2) Adenosine accumulating in the ischemic myocardium effectively suppresses exocytotic noradrenaline release by stimulating presynaptic A1-adenosine receptors. 3) Exocytotic catecholamine release ceases when the sympathetic neurons become depleted of adenosine triphosphate since this release mechanism requires high-energy phosphates. However, with progression of ischemia (i.e., greater than 10 minutes), the myocardium is no longer protected against excess adrenergic stimulation since local metabolic release mechanisms become increasingly important. This release, which is independent of both central sympathetic activation and extracellular calcium, occurs in two steps. First, catecholamines escape from their storage vesicles and accumulate in the cytoplasm of the neuron. In the second, rate-limiting step, noradrenaline is transported across the axolemma from the cytoplasm to the interstitial space via the neuronal uptake carrier in reverse of its normal transport direction. As a consequence of this nonexocytotic local metabolic release, extracellular noradrenaline reaches 100-1,000 times its normal plasma concentrations within 30 minutes of ischemia. Concentrations of this magnitude are capable of producing myocardial necrosis, even in the nonischemic heart, and may play an important role in the pathogenesis of ventricular fibrillation in early ischemia.

Animals↗
PubMed1975

The effect of clonidine and penbutolol, respectively on catecholamines in blood and urine, plasma renin activity and urinary aldosterone in hypertensive patients.

In various kinds of hypertension clonidine induced a decrease in urinary catecholamines, plasma renin activity and urinary aldosterone, concommitant with a fall in blood pressure and pulse rate in both short term and chronic studies. Furthermore, clonidine lowered the plasma levels of noradrenaline and adrenaline but a postural increase in upright position still occurred. The capacity to increase renin during salt restriction seemed mainatined. When clonidine was withdrawn all parameters returned to pretreatment levels but in some cases a marked rebound increase in catecholamine production was seen. --During clonidine the increase in catecholamines and renin after insulin induced hypoglycemia was largely abolished. Under basal conditions oral penbutolol induced a decrease of pule rate and blood pressure but no change in plasma or urinary catecholamines. During treatment plasma renin was suppressed at rest and after exercise. A work load, which led to only minor changes in blood catecholamines before treatment, was associated with a marked increase during penbutolol. Medication with penbutolol reduced the response in plasma catecholamines after hypoglycemia and renin activity remained low. Clonidine seems to act mainly by central inhibtion of symapthetic tone. Penbutolol probably acts mainly peripherally but may also have a central effect.

Adrenergic beta-Antagonists↗
PubMed1986

[Effect of beta-endorphin on catecholamine levels in the rat hypothalamus and cerebral cortex].

The present paper deals with the effect of beta-endorphin on catecholamine content in the hypothalamus and cerebral cortex of male rats. beta-endorphin was found to decrease catecholamine content in the rat brain, with the degree of reduction depending on the brain topography and the time following the peptide administration. 5 min later no changes in catecholamine content were observed either in the hypothalamus or in the cerebral cortex. 20 min later beta-endorphin induced a statistically significant fall of catecholamine concentration in the hypothalamus. A tendency towards its decrease was also observed in the cerebral cortex. 60 min later beta-endorphin produced an insignificant decrease in catecholamine level in both brain areas under study. It may be therefore suggested that beta-endorphin-induced decrease of catecholamine content in the hypothalamus and cerebral cortex represents one of the mechanisms underlying beta-endorphin stimulating action on a number of trophic functions of the hypophysis.

Animals↗
PubMed1987

Effects of chemical sympathectomy in neonatal and adult mice on C-1300 neuroblastoma tumor growth and catecholamine content.

The in situ C-1300 murine neuroblastoma (MNB) tumor model was used to investigate the influence of 6-hydroxydopamine (6HD)-induced sympathectomy on tumor growth and catecholamine concentration. One week (adult) and 3 weeks (neonatal) after sympathectomy, mice were implanted with 10(6) disaggregated MNB cells. The time interval between implantation of MNB cells and detection of palpable tumor (tumor onset time), transverse tumor diameter, tumor weight, tumor weight to body weight ratio, and tumor catecholamine concentration were determined. Sympathectomy following 6HD administration was confirmed by analysis of catecholamine concentrations in the heart and spleen by high-pressure liquid chromatography. Treatment of adult animals with 6HD reduced the mean heart and spleen norepinephrine (NE) concentrations to less than 20% of controls (vehicle treated). Neonatal sympathectomy decreased the average heart and spleen NE concentrations to less than 10% of comparable control mice. Whole brain NE and dopamine concentrations were not altered by treatment with 6HD in either age group. Tumor onset time following implantation of MNB cells was significantly increased in animals sympathectomized as either neonates or as adults. In contrast, MNB tumor growth rate following tumor onset was significantly inhibited in animals sympathectomized as neonates but not as adults. The catecholamine concentrations of tumors removed from control and sympathectomized mice 8 days after tumor onset were determined. Tumor NE and dopamine concentrations were increased 9.09 +/- 2.8- (SE) and 7.03 +/- 1.8-fold, respectively, in mice sympathectomized as neonates. There were no significant differences in the NE and dopamine concentrations of tumors obtained from sympathectomized and control adult mice. Pretreatment with desmethylimipramine prior to 6HD administration prevented destruction of sympathetic neurons, inhibition of tumor growth rate, and the increase in tumor catecholamine concentration observed in neonatally sympathectomized mice. These data suggest that the influence of chemical sympathectomy on MNB tumor growth and biochemical differentiation, as defined by catecholamine content, are age dependent.

Age Factors↗
PubMed1987

Effects of doxorubicin on the release of catecholamines from the bovine adrenal medulla.

We have studied the effects of the anthracycline doxorubicin on the release of catecholamines from the perfused bovine adrenal gland. Doxorubicin produced different concentration-dependent effects on adrenomedullary catecholamine secretion. At a 3 x 10(-6) M concentration, doxorubicin facilitated the secretory response induced by acetylcholine and 56 mM K+ but did not affect the spontaneous catecholamine output or that evoked by NaCl deprivation. Conversely, a higher concentration of doxorubicin (10(-4) M) resulted in a significant and irreversible inhibition of the spontaneous secretion of catecholamines, as well as of that caused by acetylcholine or high K+. Doxorubicin at this high concentration did not modify the catecholamine release induced by NaCl deprivation. These results suggest that doxorubicin effects could be mediated at the plasma membrane of the chromaffin cells. The present study is compatible with the idea that increased adrenomedullary catecholamine release is involved in the cardiotoxic action of relatively low doses of doxorubicin.

Acetylcholine↗
PubMed1982

The ethanol withdrawal syndrome in the rat: effects of drug treatment on adrenal gland and urinary catecholamines.

It has been found that a short period of severe intoxication with ethanol produces a marked reduction of adrenal catecholamines. Animals so treated demonstrate moderate to severe withdrawal signs. Accordingly, adrenal and urinary catecholamines were determined in rats undergoing withdrawal after treatment with several drugs known to modify sympathetic function. The depressant diazepam obtained withdrawal severity without altering peripheral catecholamines, propranolol reduced urinary catecholamines and transiently ameliorated withdrawal, whereas hexamethonium elevated urinary catecholamines and enhanced the severity of withdrawal. No drug treatment modified adrenal catecholamine levels. In this model the attenuation of adrenergic function has no consistent influence on the manifestation of withdrawal after ethanol.

Adrenal Glands↗
PubMed1984

Inhibition of catecholamine transport into chromaffin granule ghosts isolated from bovine adrenal glands by phenytoin.

The anticonvulsant drug, phenytoin, has been reported to inhibit both the transport of catecholamines into synaptosomes and monoamine oxidase. The objective of this research was to determine whether phenytoin inhibited the transport of catecholamines into storage granules. This was tested by examining the effects of phenytoin (0.05 to 0.4 mM) on the ability of (-)-[3H] norepinephrine to be transported into chromaffin granule "ghosts" isolated from bovine adrenal glands. Our results indicated that phenytoin, but not phenobarbital, inhibited catecholamine transport in a dose-dependent manner with 50% inhibition occurring at a phenytoin concentration of 0.2 mM. Kinetic analysis of the effects of phenytoin on this transport process indicated that phenytoin was a competitive inhibitor of catecholamine transport with an approximate Ki of 0.3 mM. Furthermore, phenytoin did not inhibit the Mg adenosine triphosphatase required for providing the energy source for the catecholamine transport process, nor did it dissipate the membrane potential generated by this enzyme. The competitive inhibition of catecholamine transport produced by phenytoin is probably not related to the anticonvulsant effects of the drug as it occurred at greater than therapeutic concentrations. However, this effect may be related to the toxic effect of the drug.

Adenosine Triphosphatases↗
PubMed1984

Catecholamine sulfates and platelet phenolsulfotransferase activity in essential hypertension.

Because of high plasma concentrations of conjugated catecholamines and their unknown relationship to hypertension, we determined those conjugates more specifically as catecholamine sulfates together with the sulfoconjugating enzyme-phenolsulfotransferase activity in platelets of 62 patients with essential hypertension and 32 normal controls. Our results indicated: (1) that the pool of total (free and sulfated) catecholamines (dopamine, norepinephrine, and epinephrine) is higher (because of an increase in dopamine sulfate levels) but the degree of epinephrine conjugation is lower in patients with essential hypertension compared with controls; (2) that norepinephrine sulfate levels rise with age in both groups, but the increase in free norepinephrine with age observed in controls was not observed in patients with essential hypertension; and (3) that catecholamine conjugates were found to be exclusively sulfates and platelet phenolsulfotransferase activity was not different in both groups. Platelet phenolsulfotransferase activity was, however, positively correlated with plasma norepinephrine sulfate levels, and the degree of sulfoconjugation of norepinephrine was positively correlated with that of dopamine in controls but not in patients with essential hypertension. These abnormalities occurring in essential hypertension in the absence of intergroup differences in platelet phenolsulfotransferase activity suggest that the enzyme is either not a good marker of the overall activity or that other factors account for the observed differences. Thus, additional determinants of the process of generation and degradation of sulfoconjugated catecholamines, some of which may be more stable markers of sympathetic activity than free catecholamines, need to be explored.

Adult↗
PubMed1984

Kinetics of enzymatic O-methylation: its value in assays for catecholamines in plasma.

The kinetics of enzymatic O-methylation of catecholamines were studied under conditions like those used in the radioenzymatic assay of plasma catecholamines. Inappropriate Michaelis-Menten kinetics and linear approximations of exponential equations were not used. Mathematical analysis indicated the importance of the ratio of methyl donor (S-adenosylmethionine) to substrate (catecholamine) concentration. If the reaction is incomplete, only a large ratio will allow linear approximations between product formed and initial catecholamine concentration. The use of high-concentration internal standards to correct for plasma interference may give erroneous results by reducing this ratio. Accuracy will be improved by ensuring (a) that S-adenosylmethionine is always greatly in excess of catecholamine, (b) that concentrations of added standards are of the same order as for endogenous catecholamine, and (c) that a high activity of enzyme is used, to allow the reaction to reach completion even in the presence of some inhibition.

Catechol O-Methyltransferase↗
PubMed1984

[The factors affecting plasma catecholamines concentration in rats and man].

Rat and human plasma catecholamines were measured simultaneously by HPLC-THI, HPLC-ECD and REA, and the three methods were compared. An attempt was also made to determine the factors affecting the estimated value of plasma catecholamine concentration. Our study showed that: Sensitivity and reproducibility to norepinephrine and epinephrine were identical in all three methods. One advantage of the REA method is that comparatively smaller sample volumes are required to produce similar results. Plasma dopamine concentration in peripheral blood samples was determined by the HPLC-ECD rather than the HPLC-THI method. Withdrawal of 5 ml of blood produced a significant increase in norepinephrine, epinephrine and dopamine in rat plasma. The catecholamine concentration in these cases was determined by the REA method. Plasma norepinephrine concentration did not increase with age in Wistar Kyoto rats. However, plasma norepinephrine concentration increased significantly with age in stroke-prone spontaneously hypertensive rats (SHRSP). Plasma norepinephrine concentration in male SHRSP was greater than that in female SHRSP. SHRSP-plasma norepinephrine concentrations rose in parallel to increases in blood pressure. The plasma norepinephrine concentration in SHRSP with cerebral hemorrhage rose significantly as compared with the plasma norepinephrine levels in SHRSP without cerebral bleeding. Because each method of determination of plasma catecholamine concentration has both merits and demerits, selection should be determined by sample size and amount of catecholamines in the plasma samples. Factors affecting the estimated value of plasma catecholamine concentration should be taken into consideration.

Animals↗
PubMed1981

[Determination of plasma catecholamine as a quantitative index for the evaluation of sympathetic nervous system function in man during methacholine test (author's transl)].

For many years blood pressure has been only an index among a number of physiological conditions presenting sympathetic nervous systems activities in methacholine test due largely to the lack of specific and practical method for the determination of catecholamine. We found that methacholine induced a significant increase in plasma catecholamines with an alternation in hemodynamic change in the present study by the use of high speed liquid chromatography and automated THI method. The increments in plasma catecholamines were not correlated with apparent decrements in blood pressure. Therefore the increments in plasma catecholamines induced by methacholine were not attributable to reflex responses to hemodynamic changes and rather could be the direct effect of methacholine on sympathetic neuron and adrenal medullae. Besides there was no correlation between the increments in plasma catecholamines and methacholine indices. These data question the suitability of blood pressure as an index for the evaluation of sympathetic nervous system function during methacholine test and suggest that plasma catecholamines might be a proper parameter for the sympathetic nervous activities response to methacholine.

Adult↗
PubMed1980

Mechanisms of ionophore-induced catecholamine secretion.

A number of carboxylic ionophores stimulate the secretion of norepinephrine from cell suspensions prepared from a transplantable rat pheochromocytoma. The divalent-cation ionophore ionomycin stimulates catecholamine secretion by a mechanism that is dependent upon the presence of extracellular Ca++. It is likely that ionomycin-induced catecholamine secretion results from the ionophore-mediated entry of Ca++ into the cells. The monovalent-cation ionophore monensin stimulates catecholamine secretion by a mechanism that is independent of extracellular Ca++, but is markedly dependent upon extracellular Na+. Monensin probably transports Na+ into the pheochromocytoma cells and increases the intracellular concentration of Na+ in these cells. This rise in intracellular Na+ may cause the release of Ca++ from some intracellular store. Lasalocid stimulates catecholamine secretion by a mechanism that is independent of extracellular Ca++ and is only slightly dependent upon extracellular Na+. The action of lasalocid, in contrast to the actions of ionomycin and monensin, is potentiated by decreased pH. It is likely that lasalocid enters the cells in its uncharged, protonated form. Once inside the cells, lasalocid may promote the release of intracellular Ca++. Alternatively, lasalocid and monensin may stimulate catecholamine secretion by the process which is independent of Ca++. These experiments show that ionophores can stimulate catecholamine secretion by at least three distinct ionic mechanisms.

Adrenal Gland Neoplasms↗
PubMed1994

[Plasma catecholamine levels in patients during surgical removal of pheochromocytoma under sevoflurane anesthesia].

We measured plasma catecholamine levels and hemodynamics in 5 patients during surgical removal of pheochromocytoma under sevoflurane anesthesia. Plasma catecholamine levels were unchanged with sevoflurane anesthesia. Plasma epinephrine, norepinephrine and dopamine levels increased 149 folds, 7.8 folds and 2.9 folds respectively as compared with preanesthetic values during surgical manipulation of the tumor, and then declined in magnitude but still remained 15 folds, 2.7 folds and 1.8 folds higher respectively as compared with the preanesthetic levels after removal of the tumor. These catecholamine levels finally reached 180%, 20% and 60% of the preanesthetic values respectively after the emergence from anesthesia in the recovery room. Mean systolic and diastolic arterial blood pressures were 127/82 mmHg before anesthetic induction and increased to 211/71 mmHg during manipulation of the tumor. Then they decreased to 75/52 mmHg immediately after removal of the tumor but recovered up to 126/71 mmHg on recovery from anesthesia. Alpha and beta adrenal blockers were administered if necessary to control hypertension and tachycardia during manipulation of the tumor. Hypotension after removal of the tumor was treated with volume replacement, vasopressor and/or catecholamines. No correlation was found between plasma catecholamine levels and arterial blood pressure in our study except during manipulation of the tumor. No arrhythmias were observed during anesthesia and surgery in our cases even though plasma catecholamines increased extremely with surgical intervention. We conclude that sevoflurane anesthesia is a better choice for surgery for pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1996

SPE-HPLC determination of catecholamines using an affinity principle.

Solid-phase extraction (SPE) with the affinity chromatography principle was applied for high performance liquid chromatography (HPLC) determination of catecholamines in patients urine samples. Electrochemical amperometric detection (ED) was used for all HPLC analyses and both analytical and microbore columns were tested for optimal chromatographic resolution of all analyzed catecholamines. Capacity ratio k' and detection limits were evaluated for all columns used. Precolumn affinity chromatographic procedure of catecholamines with diphenylboronic acid (DPBA) in alkaline medium improved their retention on different commercial SPE reversed-phase cartridges. After clean-up and preconcentration step the complex catecholamine-diphenylboronic acid was degraded by acidic pH and eluted from SPE cartridge. After SPE affinity step catecholamines were analyzed by HPLC-ED. The optimal elution solutions was chosen also as suitable SPE cartridges. Extraction recoveries of catecholamines were 89.6-93.3% with relative standard deviation RSD = 3.8-4.3%. Total analysis time was 30 min including 15 min for the preseparation procedure.

Boron Compounds↗
PubMedDate not supplied

[Catecholamines, their precursors and metabolites in human fatigue after exertion].

Alterations in metabolism of catecholamines were studied in sportsmen after development of acute fatigue as a result of the test physical loading. Three types of the alterations were characterized on the basis of differences in excretion with urine of free and sulphate-bound adrenaline, noradrenaline, of their precursors DOPA and dopamine as well as acid metabolites (vanillyl mandelic acid). The first type of the alterations in catecholamines metabolism comprized the cases, when excretion of catecholamines, their precursors and metabolites did not increase; this appears to relate to the partial exhaustion of hormones and peripheric mediators of sympathoadrenal system. The second type was characterized by decreased excretion of the substances studied, by development of the "perversed" reactions due to modifications in the regulatory system, which led to the inhibition of the system instead of its stimulation. The third type was manifested as the hyperfunction of the system. The increased synthesis of catecholamines during the hyperfunction suggests that this process serves as a compensatory reaction to their preceding elevated secretion; the phenomenon appears to depend on the increased secretion of the newly formed catecholamines. Excretion of catecholamines and their precursors was decreased for a long time after development of chronic fatigue in the resting state and the increase in excretion of the substances studied was not observed after physical loading.

Adolescent↗