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At least 1,531 records · Page 85Linked to original sources
PubMed1985

Catecholamines in arterial and venous umbilical blood: placental extraction, correlation with fetal hypoxia, and transcutaneous partial oxygen tension.

In 34 parturient women the levels of free epinephrine (E), norepinephrine (NE), and dopamine (D) were determined by a radioenzymatic method using maternal venous and umbilical arterial and venous blood. The study was conducted to investigate the relationship between fetal catecholamines and hypoxia, fetal heart rate (FHR), and transcutaneous pO2 (tcpO2). The placental catecholamine extraction rates were also calculated. Results The NE concentrations (10,200 pg/ml) and the E concentrations (1,120 pg/ml) in the fetal arterial blood were highly elevated with mean values increased 4-fold over umbilical vein values. Compared with the maternal venous blood, NE values were increased 20-fold, and E values 10-fold. Free D concentrations in fetal arterial blood (130 pg/ml) had risen 2.5-fold over maternal levels. These results suggest that the catecholamines measured in cord blood are of fetal origin and that the placenta has a high capacity for inactivation of free catecholamines. The placental extraction rate is 77 +/- 14% for NE, 76 +/- 16% for E, and 33 +/- 25% for D. The placental extraction rates for E and NE were virtually identical; in agreement with morphological studies they demonstrated absence of sympathetic innervation on the fetal side of the placenta. Highly significant correlations were found between fetal arterial NE concentrations and the 1-minute APGAR score, pH and base deficit in the umbilical artery and alterations of the FHR (deceleration area, baseline FHR). Further analysis of FHR alterations reveals that an increase in deceleration area without tachycardia is not correlated with an increase of fetal arterial NE concentration. A significant rise in NE was only found with additional tachycardia which is often associated with a loss of oscillation amplitude. Fetal arterial E concentrations were found to correlate with the fetal parameters indicating increased adrenal secretion of the hormone during fetal stress. However, correlation coefficients were lower than those obtained for NE. A significant effect of fetal hypoxia on arterial and venous D levels could not be demonstrated. Fetal tcpO2 varies between 0-25 mm Hg during the last two hours before delivery. In most cases tcpO2 was lower than the arterial pO2. Besides epidermal thickness and artifacts, skin perfusion is a major factor influencing the tcpO2 (transcutaneous arterial pO2 difference). Vasoconstriction of the cutaneous vessels induced by increased NE secretion during hypoxia may obviously produce a fall in tcpO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Plasma vasopressin, renin and catecholamines during nitroprusside-induced hypotension in the newborn lamb.

The circulating levels of vasopressin, catecholamines and renin activity before, during and following a 10-20% fall in mean arterial blood pressure induced by sodium nitroprusside were measured in six chronically catheterized lambs during the first week of life. No significant changes in pHa, PaO2, PaCO2, Plasma sodium or osmolality were observed during or following the infusion of sodium nitroprusside at an average of 12 g.kg-1.min-1 (table I). However, the fall in blood pressure at the end of 60 minutes infusion, was associated with significant increases in the plasma levels of vasopressin from a control value of 2.4 +/- 0.57 to a maximum of 35.1 +/- 16.3 pg/ml (p = .002), renin activity from 6.7 +/- 1.56 to 27.4 +/- 11.44 ng.ml-1.hr-1 (p = .003), and catecholamines from 189.3 +/- 42.15 to 543.3 +/- 100.52 pg.ml-1 (p = .0001). The increase in vasopressin is lower, while that of PRA was higher and catecholamines similar to those found in the ewe. Plasma renin activity (PRA) and catecholamine levels remained elevated for at least 30 minutes following the end of the infusion while the mean blood pressure rose significantly above control levels and remained elevated for twenty minutes. We speculate that the persistent elevated levels of vasoactive mediators are responsible for the prolonged rebound hypertension following the cessation of the nitroprusside infusion and is the result of an immaturity of either a feedback process or metabolism of the vasoactive mediators or a combination of both mechanisms. This rebound hypertension could have adverse effects particularly in the very immature neonate.

Animals↗
PubMed1996

Fetal and maternal catecholamine levels at delivery.

The objective of this study was to investigate any relationships between maternal and fetal catecholamine levels and clinical labour outcomes. Patients were a subgroup of healthy primigravid women who were enrolled for a randomized controlled trial of labour companionship and who had blood samples for catecholamines at delivery. Norepinephrine, epinephrine and dopamine were determined by high performance liquid chromatography. There were no significant correlations between the maternal and fetal catecholamine levels and labour duration. Fetuses who had umbilical artery base excess < -10 had significantly higher epinephrine (p = 0.03) and dopamine (p = 0.02) levels and those who had a pH less than 7.2 had significantly higher dopamine (p = 0.02) levels. These results confirm a high fetal catecholamine response to hypoxia.

Adolescent↗
PubMed1989

The role of catecholamines in estradiol and progesterone secretion by cultured explants and cells of human term placentae.

The effects of physiological concentrations of the native catecholamines norepinephrine and epinephrine upon term placental hormonal function were examined by measuring estradiol and progesterone secretion by organ and cell culture systems. Results show that, in explants, both catecholamines caused a significant increase in the secretion of both sex steroids, p less than 0.05. Estradiol secretion was blocked by the alpha and beta adrenergic receptors antagonists, phenoxybenzamine and propranolol, respectively, p less than 0.05. Norepinephrine but not epinephrine dependent progesterone secretion was blocked by propranolol. In cells, epinephrine stimulated cyclic AMP generation and caused a 30% increase in estradiol secretion, p less than 0.05. Both were abrogated by propranolol. Norepinephrine increased secretion by 25%, p less than 0.05. This was inhibited by yohimbin and prazosin, alpha-1 and -2 receptors antagonists, respectively. In conclusion, the placenta in vitro is a target organ for catecholamines. The marked response of the explant system as compared with the marginal response of the cell culture system indicates that cell to cell contact/communication is required for full expression of catecholamine effect.

Adrenergic alpha-Antagonists↗
PubMed1992

Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors.

Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.

Animals↗
PubMed1994

Low cord blood levels of catecholamine from a newborn of a pheochromocytoma patient.

Association of pheochromocytoma and pregnancy is rare and usually related to high maternal and fetal mortality rates. Maternal effects of the tumor have been studied extensively and the clinical outcome has markedly improved during the last decade. However, the role of excess catecholamines on fetal development has been discussed very little. We report here a case of pheochromocytoma during pregnancy. In which catecholamine levels from the cord blood were low despite simultaneous elevated maternal values (1.93 and 29.46 nmol/l norepinephrine, respectively), possibly owing to the high activity of the catecholamine degradative enzymes monoamine oxidase and COMT at the placental level. We suggest that in pregnancies complicated by pheochromocytoma, fetal well-being may be related mainly to good control of maternal blood pressure instead of the amount of catecholamines in the fetal circulation, because the placenta performs a protective role through an effective process of hormone inactivation.

Adrenal Gland Neoplasms↗
PubMed1979

Responses of the transmembrane potential coupled to the ATP-evoked catecholamine release in isolated chromaffin granules.

Using suspensions of chromaffin granules isolated from bovine adreno-medullae, the effects of Mg2+.ATP on membrane potential and catecholamine release across membranes of granules were investigated. The release of catecholamine was monitored by the measurement of changes in endogenous fluorescence of the amines, while the fluorometric method with 3,3'-dipropylthiadicarbocyanine iodide (diS-C3-(5)) was applied to the measurement of membrane potential changes. The catecholamine release brought about by Mg2+.ATP was found to obey Michaelis-Menten kinetics with Km-value for Mg2+ of about 0.15 mM and to be inhibited by dicyclohexylcarbodiimide (DCCD), an inhibitor of membrane-bound H+-ATPase. Concomitantly with such an amine release, depolarization of the granule membrane was observed to occur. The magnitude of this depolarization closely paralleled with the rate of the amine release and followed a saturation kinetics of Michaelis-Menten type with Km for Mg2+ of 0.21 mM and for ATP of 0.22 mM. Moreover, such a depolarization was competitively suppressed by DCCD. Based on these results, the role of the transmembrane potential change of granules in the catecholamine release was discussed.

Adenosine Triphosphate↗
PubMed1984

Operation of internal Na-dependent Ca influx mechanism associated with catecholamine secretion in the adrenal chromaffin cells.

The cat adrenal gland was retrogradely perfused with a medium lacking divalent cation, and the secretion of catecholamines was induced by Ca reintroduction with or without simultaneous removal of external Na. These responses were markedly reduced after prior exposure to a medium containing Mg (1 mM) or lacking Na. The inhibition caused by Mg was reversed by ouabain treatment. Reversing the concentration gradient for Na alone by replacing external Na with Tris, choline, or Li did not stimulate catecholamine secretion when Ca2+ (0.1 mM) was present in the external medium throughout the experiment. However, the treatment with ouabain reversed this inhibitory effect of Ca so that Na removal did induce marked secretion. Essentially similar results concerning secretion were obtained in the cultured bovine chromaffin cells. There was a reasonable correlation between secretion and 45Ca uptake in these cells under various experimental manipulations, and alterations of these parameters were well correlated with the level of internal Na. Furthermore, the rate constant of 22Na efflux was found to increase when Ca was reintroduced with the simultaneous removal of Na during exposure to a medium containing ouabain. These results are consistent with the view that the mechanism of internal Na-dependent Ca influx is activated to induce catecholamine secretion whenever internal Na is raised above a critical level. On the other hand, there were significant increases in the catecholamine secretion and 45Ca uptake which were induced by substitution of NaCl with sucrose, even when the operation of the internal Na-dependent Ca influx mechanism was markedly restricted by various experimental manipulations. This suggests that other secretory mechanisms are involved under these conditions. This would account for the largest secretory effect of sucrose substitution under the condition in which internal Na-dependent Ca influx is activated.

Adrenal Medulla↗
PubMed1996

The roles of catecholamines in glucoregulation in intense exercise as defined by the islet cell clamp technique.

Exercise at > 85% VO2max causes the greatest known physiological increases in glucose production rates (Ra). To define the relative roles of catecholamine versus glucagon/insulin responses in stimulating Ra, normal subjects in the postabsorptive state exercised at 87 +/- 2% VO2max during an islet cell clamp (IC): intravenous octreotide (somatostatin analog), 30 ng.kg-1.min-1; glucagon, 0.8 ng.kg-1.min-1; growth hormone, 10 ng.kg-1.min-1; and insulin adjusted to achieve euglycemia, then constant 56 +/- 7 min before exercise. Seven control subjects exercised without an IC. In four subjects (IC-1) with hormone infusions held constant during exercise, plasma insulin rose 76% and glucagon 35%, perhaps because of altered hemodynamics. In seven subjects (IC-2), hormone infusions were decreased stepwise during exercise and returned stepwise to initial rates during early recovery. Ra increased sixfold in control and both IC groups. Plasma norepinephrine and epinephrine likewise increased > 12-fold with no differences among groups; both catecholamines correlated closely with Ra. Because mixed venous blood plasma insulin declined and glucagon did not change in control subjects, the glucagon-to-insulin ratio increased from 0.20 to 0.26 (P = 0.02). In IC subjects, plasma insulin increased and glucagon was either constant (IC-2) or increased less than insulin, resulting in nonsignificant declines in the immunoreactive glucose-to-immunoreactive insulin ratio. Although a rise in insulin would have been expected to attenuate the Ra increment, this effect was overridden. The strong correlations of Ra with catecholamines and the similar Ra responses despite divergent glucagon-to-insulin responses are consistent with the primacy of catecholamines in regulation of Ra in intense exercise.

Adult↗
PubMedDate not supplied

Differential effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion.

The effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion were compared in normal men to search for possible hypothalamic or pituitary inhibitory effects of proinsulin on glucocounterregulatory responses. When subjects received 0.1 U/kg i.v. human insulin and 25-38 micrograms/kg i.v. human proinsulin on separate occasions, plasma glucose decreased more rapidly after insulin, and the nadir was slightly lower, but integrated hypoglycemic responses were similar. Cortisol, growth hormone (GH), prolactin, epinephrine, and norepinephrine responses occurred more rapidly after insulin than after proinsulin. Peak and integrated cortisol, GH, and catecholamine responses to insulin and proinsulin were similar, but those of prolactin were reduced after proinsulin when compared with insulin by 42% (P less than .01) and 34% (P less than .05), respectively. When euglycemia was maintained by a variable glucose infusion rate after the injection of insulin and proinsulin, no differences were observed in plasma levels of any of the hormones. The intravenous injection of a dose of proinsulin (6 micrograms/kg), which did not produce hypoglycemia but was the molar equivalent of insulin used in the first protocol, failed to modify the GH or prolactin responses to a combined injection of GH-releasing hormone (1 microgram/kg) and thyrotropin-releasing hormone (500 micrograms). Our results indicate that the onset of pituitary hormone and catecholamine responses to hypoglycemia are related to the rate of plasma glucose decline, with the slower responses to proinsulin reflecting a more gradual onset of hypoglycemia. The magnitude of the cortisol, GH, and catecholamine responses, however, was comparable with proinsulin- and insulin-induced hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of mood states, smoking and urinary catecholamine excretion on hemoglobin A1c in male Japanese workers.

To know the association between psychological strain and glycosylated hemoglobin (HbA1c) and to examine roles of smoking and catecholamine excretion as a possible mediator in the association, we measured mood states (Profile of Mood States, POMS), urinary catecholamines (adrenalin, noradrenaline and dopamine) from urine sample in early morning, HbA1c and fasting plasma glucose (FPG) of 63 male employees on a rest day. After excluding 12 subjects who had diabetes or impaired glucose tolerance or had missing response to the questionnaire, data from 51 subjects were analyzed. The POMS anger-hostility score significantly and positively correlated with HbA1c (p < 0.05), while other scale scores did not (p > 0.05). Number of cigarettes smoked per day significantly and positively correlated with HbA1c (p < 0.05). Urinary excretion rate of any catecholamine did not significantly correlate with HbA1c (p > 0.05). Multiple linear regression analysis indicated that the anger-hostility score significantly correlated with HbA1c after controlling for number of cigarettes per day (p < 0.05). It is suggested that, among mood states, anger-hostility is associated with increased HbA1c. However, our study failed to find a mediating role of urinary catecholamines or smoking on the association between the mood and HbA1c.

Adult↗
PubMed1996

Effects of earplugs on catecholamine and cortisol excretion in noise-exposed textile workers.

To investigate physiological and psychological effects of industrial noise, a survey was performed on 50 female workers exposed to machinery noise [93-100 dB(A)] (noise group) and 25 female workers in less-noisy environments [71-75 dB(A)] (control group) in a textile factory in Vietnam. Urine was collected for analysis of catecholamines and cortisol. The subjects were also asked to fill out a questionnaire. Each subject was examined over 2 working days. The workers in the noise group were asked to put earplugs in their ears during the working hours of the 2nd day. On the 1st day without earplugs, urinary excretion of catecholamines in the noise group were greater than those in the control group. Cortisol in urine showed a similar tendency. Differences in catecholamine excretion between the noise group and the control group decreased on the 2nd day when the earplugs were used for attenuation of noise level in the noise group. Frequency of subjective fatigue symptoms was lower on the 2nd day than that on the 1st day in noise group, while the control group showed almost no day-difference. The results indicate that the catecholamine response to noise in workers was reduced through the use of earplugs.

Adult↗
PubMed1999

The effect of nicotine on developing brain catecholamine systems.

Biochemical studies have confirmed that nicotinic acetylcholine receptor mRNA and protein are expressed early in the development of the fetal central nervous system. Perinatal administration of nicotine produces a broad spectrum of effects on brain development, including inhibition of DNA synthesis, altered ornithine decarboxylase activity, altered neurotransmitter function, and significant alterations in cortical morphogenesis. Catecholamine systems, both in the brain and in the periphery, are particularly sensitive to prenatal nicotine exposure. Acute and chronic nicotine administered to pregnant dams causes alterations in dopamine and its metabolites in male and female rat fetuses. These changes can persist into adulthood. Prenatal nicotine exposure also causes locomotor disturbances in pups, which can have long-lasting effects. The effect of nicotine on developing noradrenergic neurons is less clear. Some effects may include increases in noradrenergic neuronal activity in the pup and aberrant central release of norepinephrine in response to neonatal hypoxia after nicotine exposure in utero. Catecholamine neurons develop early in ontogeny, so nicotine induced alterations have the potential to induce permanent changes. Hence, more research is needed to get a clearer picture of the effect of nicotine on developing catecholamine systems. The affects of nicotine on catecholamine systems in the adult are discussed for comparison.

Animals↗
PubMed1980

Stability of human plasma catecholamines.

Human plasma catecholamines, measured by a radioenzymatic method, in general exhibit a marked stability when stored in plasma or whole blood. The storage of blood samples for several hours at room temperature, without prior separation of plasma, did not result in any losses of plasma noradrenaline or adrenaline. Moreover, the addition of thiol compounds (such as reduced glutathione, 2-mercaptoethanol or dithiothreitol) or other antioxidants (sodium metabisulphite) was not required during the storage. Although catecholamines were stable when kept in whole blood at room temperature, they were swiftly degraded when stored in buffer solutions in the absence of thiols. In one subject adrenaline and noradrenaline were repeatedly found to increase significantly in concentration in the course of the first 30 min of storage. The reason for this anomalous increase is unknown. The observed stability of catecholamines in blood is in striking contrast to some earlier reports. It appears to be premature to categorically neglect any precautions as regards the centrifugation, sampling and processing blood samples used for plasma catecholamine determinations; however, when a given routine method is employed one may check the apparent stability of noradrenaline and adrenaline. In some cases this may justify omitting some of the tedious and expensive arrangements suggested in the literature for sample processing.

Adult↗
PubMed1985

Effect of different denervation procedures on catecholamines in the gut.

Sympathectomy has been used to study the role of the sympathetic nervous system in the control of gastric acid secretion. Conflicting results may reflect differences in the sympathectomy procedures used. In a previous study we showed a reduction of catecholamines by more than 90% in the gut wall of the rat after surgical upper abdominal sympathectomy. The aim of the present investigation was to ascertain whether chemical sympathectomy was equally effective and whether total denervation, including combined chemical and surgical sympathectomy together with bilateral truncal vagotomy, would lower the catecholamine levels further. The results showed that chemical sympathectomy reduced noradrenaline levels in fundus (oxyntic) and antrum mucosa to levels similar to those after surgical sympathectomy (less than 5%), but the reduction was less pronounced in the muscle layer of the fundus and antrum and in the pancreas and spleen. Combined surgical and chemical sympathectomy did not reduce noradrenaline more effectively than surgical sympathectomy alone. Vagotomy reduced catecholamines in the stomach by about 50%; in extragastric tissues vagotomy was without effect. Total denervation, including combined surgical and chemical sympathectomy plus vagotomy, did not reduce noradrenaline levels more than surgical sympathectomy alone, suggesting that the proportion of adrenergic fibers that derive from the vagus is quantitatively insignificant but that the vagus exerts a local control of the sympathetic stores of gastric catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Aqueous humor catecholamines.

The catecholamines norepinephrine, (NE) epinephrine (E) and dopamine (DA) were detected for the first time in the aqueous humor of humans under general anesthesia and monkeys under ketamine. The catecholamine levels in aqueous humor of 9 humans were assayed. NE was 0.796 +/- 0.457 ng./ml., E ranged between 0 and 0.132 ng./ml. in 4 out of 9 subjects, and DA was found in 2 of the 9 eyes. (0. 123ng ./ml. and 0. 318ng ./ml..) Plasma levels were measured in 8 of the human subjects at the time of aqueous sampling -NE was 0.311 +/- 0.171, E ranged between 0 and 0.097 (4 out of 8 subjects) and DA was detected in one subject- 0.037 ng./ml.. Monkey aqueous levels were NE:2.843 +/- 0.668 and DA:0.462 +/- 0.177 ng./ml., with an intact iris. (N = 8 eyes.) NE was 0.497 +/- 0.049, and DA 0.426 +/- 0.218 ng./ml. after total iridectomy. (N = 4 eyes) E was not detected in the monkey under these conditions. Whilst NE may be produced in part by the iris, DA levels were not affected by iridectomy. This implies that DA may be produced by structures unrelated to sympathetic nerve endings of the iris in the anterior segment of the non-human primate eye, perhaps by diffusion from the ciliary body or retina. Ketamine is known to inhibit catecholamine uptake, which may explain the high levels measured in the monkey. Human aqueous catecholamine levels measured under anesthesia may be affected by a variety of the drugs used. It is postulated that dopaminergic neurones and associated receptors may be present in the anterior segment of the eye. This may explain the presence of aqueous humor dopamine and the effects of dopaminergic drugs on intraocular pressure.

Adult↗
PubMedDate not supplied

Basal catecholamine and cortisol secretion in primary chromaffin cell cultures before and after purification and retroviral transfection.

We have investigated the effects of supraphysiological concentrations of catecholamines on glucocorticoid secretion in vitro. These effects were analyzed in adrenocortical cells shown to be present in chromaffin cell cultures as well as in cortical cells cocultured with transfected chromaffin cells that overproduce catecholamines. Cortisol release from residual cortical cells in chromaffin cell cultures was found to be 2.5 times higher than from isolated adrenocortical cells. Removal of the adrenocortical cells from the chromaffin cells resulted in an almost complete cessation of cortisol secretion. Catecholamine overproduction was achieved by transfecting chromaffin cells with the blank retroviral vector pSAM-EN. Coculture of adrenocortical cells with these transfected chromaffin cells further enhanced the stimulating effect of chromaffin cells on cortisol 2.3-fold compared to normal cocultures. In conclusion, cortical cells in chromaffin cell cultures secrete significant amounts of cortisol, which should be considered when evaluating the endocrine function of these cell cultures and which can be abolished by purification. The hormonal activity of adrenocortical cells is highly increased in an environment of catecholamine overproduction, which is of both basic and clinical importance.

Adrenal Cortex↗
PubMed1999

Increased plasma atrial natriuretic factor in catecholamine-producing tumor patients.

The aim of this study was to evaluate plasma levels of ANF in patients with catecholamine-secreting tumors with and without hypertension and to relate ANF secretion to levels of plasma and urinary catecholamines and blood pressure. Twenty-one pheochromocytoma (15 with sustained, 6 with paroxysmal hypertension), 6 neuroblastoma (1 hypertensive) patients and 28 aged-matched controls were studied in basal conditions. Plasma and urinary norepinephrine (NE),epinephrine (E), dopamine (DA) and DOPA were determined by HPLC-ED and plasma ANF by RIA. Both neuroblastoma and pheochromocytoma patients had significantly higher plasma ANF levels than controls. Neuroblastomas showed higher ANF concentration than pheochromocytomas. No differences were found in plasma ANF between hypertensive and normotensive patients. Pheochromocytomas with ANF levels within the normal range had plasma and urinary NE and urinary DA and DOPA levels significantly higher than patients with high ANF. Plasma ANF levels were unrelated to systolic or diastolic blood pressure or heart rate. A negative correlation between plasma ANF and urinary DA was found only in the patients groups. In conclusion, plasma ANF was increased in pheochromocytoma and neuroblastoma patients. Our data suggest that the excessive catecholamine secretion is not responsible for the increased ANF secretion in these patients. The significance of the relationships among plasma ANF and urinary and plasma catecholamines requires further investigation.

Abdominal Neoplasms↗