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At least 937 records · Page 52Linked to original sources
PubMed1990

Catecholamines depress endolymphatic sac direct current potential in guinea pigs.

To test the possibility that catecholamines have an influence on the function of the endolymphatic sac (ES), which is known to absorb the endolymph, the effect of catecholamines on the ES direct current potential (ESP) was examined in the guinea pig. The ESP was recorded extradurally by the posterior occipital approach. Isoproterenol (Iso), epinephrine (Epi), and norepinephrine (NE) were administered intravenously for 4 min using an infusion pump. Catecholamines reversibly depressed the ESP with the rank order of potency Iso greater than Epi greater than NE. The threshold doses were 0.021, 0.27, and 1.94 micrograms/kg for Iso, Epi, and NE, respectively. beta-Antagonist (propranolol) blocked the action of catecholamines on the ESP but alpha-antagonist (phentolamine) did not. This indicates that beta-adrenergic action induces the ESP change. This study implies that catecholamines may regulate the function of the ES.

Adrenergic beta-Antagonists↗
PubMed1995

Correlation between neural release of VIP and adrenomedullary catecholamine secretion in vivo.

The aim of the present study was to determine whether vasoactive intestinal peptide (VIP) can be released along with catecholamines from the adrenal gland in response to direct splanchnic nerve stimulation in anesthetized dogs. An attempt was made to verify whether VIP was released mainly from chromaffin cells or from the splanchnic nerve terminals. The first group received a supramaximal stimulation (12 V) given on the left splanchnic nerve at three successive frequencies of 0.2, 2, and 20 Hz. The second group received increasing doses of 1,1-dimethyl-4-phenylpiperazinium (DMPP) locally infused into the denervated left adrenal gland. In response to nerve stimulation, adrenal venous catecholamine concentration significantly increased in a frequency-dependent manner, whereas VIP-like immunoreactive substance (VIP-ir) reached a significant level only at the highest frequency. The multiple linear regression analyses revealed that the net increases in adrenal venous catecholamine concentrations were strongly correlated with combined variables of VIP-ir concentration and frequencies, indicating r = 0.915 and 0.949 (n = 42, P < 0.0001) for epinephrine and norepinephrine concentrations, respectively. In response to local DMPP infusion, adrenal venous catecholamines increased in a dose-dependent manner, whereas VIP-ir remained unchanged. The results indicate that VIP-ir is released along with catecholamines from the dog adrenal gland in response to direct splanchnic nerve stimulation in vivo. The study also suggests that VIP is mainly released from splanchnic nerve endings.

Adrenal Medulla↗
PubMed1992

Plasma Met-enkephalin and catecholamine responses to intense exercise in humans.

Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.

Adult↗
PubMed1989

Combined vital dye labelling and catecholamine histofluorescence of transplanted ciliary ganglion cells.

We have utilized the carbocyanine dye, DiI, to label suspensions of dissociated ciliary ganglion cells removed from 6 to 12 day old quail embryos. Some of the cells were injected into the trunk somites of 2.5-3 day old chick embryos along pathways where neural crest cells migrate to form sensory and sympathetic ganglia, aortic plexuses and the adrenal medulla; the remainder of the cells were cultured to check their viability and the persistence of the DiI label. Embryos were incubated for 1-8 days post-injection, fixed in 4% paraformaldehyde/0.25% glutaraldehyde and processed for cryostat sectioning. DiI-labelled cells were readily identifiable in culture and in sections of embryos at all stages examined. Several cell types were identified, based on their morphology and soma size. These included cells with large cell bodies and bright DiI-labelling that appeared to be neurons and smaller, more weakly labelled cells that appeared non-neuronal. The latter presumably had divided several times, accounting for their reduced levels of dye. Many of the DiI-labelled cells were found in and around neural crest-derived sympathetic ganglia, aortic plexuses and adrenomedullary cords, but were rarely observed in dorsal root ganglia. The aldehyde fixative (Faglu mixture) used in this study reacts with catecholamines to form a bright reaction product in adrenergic cells including those in the sympathetic ganglia and the adrenal medulla. The catecholamine biproduct and the DiI in the same cell can easily be viewed with different fluorescent filter sets. A variable number of the DiI-labelled cells in these adrenergic sites contained catecholamines. Cells derived from younger 6 day ciliary ganglion dissociates exhibited detectable catecholamine neurotransmitters earlier and more frequently than those derived from 8 day embryos. The presence of cells exhibiting both bright DiI and catecholamine fluorescence is consistent with previous indications that post-mitotic ciliary ganglion neurons can undergo phenotypic conversion from cholinergic to adrenergic when transplanted to the trunk environment.

Animals↗
PubMed2001

Dorsal and ventral medullary catecholamine cell groups contribute differentially to systemic interleukin-1beta-induced hypothalamic pituitary adrenal axis responses.

Medial parvocellular paraventricular corticotropin-releasing hormone (mPVN CRH) cells are critical in generating hypothalamic-pituitary-adrenal (HPA) axis responses to systemic interleukin-1beta (IL-1beta). However, although it is understood that catecholamine inputs are important in initiating mPVN CRH cell responses to IL-1beta, the contributions of distinct brainstem catecholamine cell groups are not known. We examined the role of nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) catecholamine cells in the activation of mPVN CRH, hypothalamic oxytocin (OT) and central amygdala cells in response to IL-1beta (1 microg/kg, i.a.). Immunolabelling for the expression of c-fos was used as a marker of neuronal activation in combination with appropriate cytoplasmic phenotypic markers. First we confirmed that PVN 6-hydroxydopamine lesions, which selectively depleted catecholaminergic terminals, significantly reduced IL-1beta-induced mPVN CRH cell activation. The contribution of VLM (A1/C1 cells) versus NTS (A2 cells) catecholamine cells to mPVN CRH cell responses was then examined by placing ibotenic acid lesions in either the VLM or NTS. The precise positioning of these lesions was guided by prior retrograde tracing studies in which we mapped the location of IL-1beta-activated VLM and NTS cells that project to the mPVN. Both VLM and NTS lesions reduced the mPVN CRH and OT cell responses to IL-1beta. Unlike VLM lesions, NTS lesions also suppressed the recruitment of central amygdala neurons. These studies provide novel evidence that both the NTS and VLM catecholamine cells have important, but differential, contributions to the generation of IL-1beta-induced HPA axis responses.

Adrenal Glands↗
PubMedDate not supplied

Catecholamine clearance from alveolar spaces of rat and human lungs.

BACKGROUND: Although aerosolized beta-adrenergic agonists have been used as a therapy for the resolution of pulmonary edema, the mechanisms of catecholamine clearance from the alveolar spaces of the lung are not well known. OBJECTIVE: To determine whether catecholamine clearance from the alveolar spaces is correlated with the fluid transport capacity of the lung. METHODS: Albumin solution containing epinephrine (10(-7)M) or norepinephrine (10(-7)M) was instilled into the alveolar spaces of isolated rat and human lungs. Alveolar fluid clearance rate was estimated by the progressive increase in the albumin concentration over 1 h. Catecholamine clearance rate was estimated by the changes in catecholamine concentration and alveolar fluid volume over 1 h. RESULTS: The norepinephrine clearance rate was faster than the epinephrine clearance rate in the rat and human lungs. In the rat lungs, amiloride (a sodium channel blocker) caused a greater decrease in alveolar fluid clearance and epinephrine clearance rate than propranolol (a nonselective beta-adrenergic antagonist). Although propranolol and phentolamine (an alpha-adrenergic antagonist), and 5-(N-ethyl-N-isoprophyl)amiloride (a Na+/H+ antiport blocker) changed neither the alveolar fluid clearance nor the norepinephrine clearance rate, amiloride and benzamil (a sodium channel blocker) decreased both clearance rates. As in the rat lungs, amiloride decreased alveolar fluid and norepinephrine clearance rates in the human lungs. CONCLUSION: These results indicate that the catecholamine clearance rate from the alveolar spaces is correlated with alveolar fluid clearance in rat and human lungs.

Adrenergic alpha-Agonists↗
PubMed1996

Catecholamines and indoleamines in the central nervous system of a urodele amphibian: a microdissection study with emphasis on the distribution of epinephrine.

Individual brain nuclei and regions of the central nervous system of adult male roughskin newts (Taricha granulosa) were microdissected, and the concentrations of norepinephrine, epinephrine, 3,4-dihydroxyphenylacetic acid, dopamine, 5-hydroxyindoleacetic acid, and serotonin were determined using high performance liquid chromatography (HPLC) with electrochemical detection. The pattern of distribution of these catecholamines and indoleamines revealed many similarities between this urodele and other vertebrates. The highest concentrations of biogenic amines were observed in brainstem, hypothalamic, and basal forebrain structures; the lowest concentrations were observed in the internal granule layer of the olfactory bulb and pallial structures of the telencephalon. High concentrations of catecholamines and indoleamines were found in hypothalamic periventricular regions that are known to include cerebrospinal fluidcontacting, monoamine-containing neuronal cell bodies. The rostral diencephalon, which included the preoptic recess organ, had high concentrations of the primary catecholamines, norepinephrine and dopamine, and extremely high concentrations of the secondary catecholamine epinephrine. The dorsomedial infundibular hypothalamic region, which included the paraventricular organ, had high concentrations of dopamine and serotonin. The lateral infundibular hypothalamic region, which included the nucleus infundibularis dorsalis, had high concentrations of each of the biogenic amines. The results revealed unique patterns of distribution for each of the catecholamines and indoleamines studied, and provided evidence that regions of the hypothalamus that include cerebrospinal fluid-contacting, monoamine-containing neuronal cell bodies are focal regions for the metabolism of multiple biogenic amines.

Animals↗
PubMed1985

Altered catecholamine innervation of the supraoptic nucleus in the nephrogenic diabetes insipidus mouse.

Fluorescence histochemical and immunocytochemical techniques were used to investigate morphologic correlates of the relationship between catecholamine varicosities and vasopressin-containing perikarya in an animal model of vasopressin excess, the nephrogenic diabetes insipidus mouse. Our results show hypertrophy and increased immunoreactivity in vasopressin neurons in these mice were accompanied by a marked increase in the density and to some extent the fluorescence intensity of catecholamine varicosities within the supraoptic nucleus. These results further support the concept of functional interactions between catecholamine and vasopressin neurons and raise the possibility that the target neuron, or one of its products, perhaps vasopressin, either exerts a trophic influence on the catecholamine innervation pattern of the supraoptic nucleus or enhances catecholamine content in existing fibers and terminals.

Animals↗
PubMed1987

Estimation of catecholamine potencies on the myocardium by means of a new method.

A simple method is described for evaluating the potencies of catecholamines on the slow response of myocardium. Catecholamines depolarize guinea pig ventricular muscle cells exposed to the high K+ (27 mmol/l) Tyrode's solution containing 0.2 mmol/l Ba through an increase in slow channel conductance. Higher concentrations of catecholamines in addition induce spontaneous action potentials. This model was used to estimate and compare catecholamine potencies on myocardium. Catecholamine concentrations needed for depolarization alone or for depolarization plus automatic activity were taken as basis for comparison. The order of potency obtained by means of this new method was: l-isoproterenol greater than l-adrenaline greater than or equal to dl-noradrenaline greater than or equal to dobutamine greater than or equal to dopamine. This is similar to the order reported with other methods.

Action Potentials↗
PubMed1990

Is physiologic sympathoadrenal catecholamine release exocytotic in humans?

In cultured cells and isolated perfused organs, catecholamines are coreleased with chromogranin A (CgA) from adrenal chromaffin cells and sympathetic neurons. The corelease suggests that exocytosis is the mechanism of catecholamine secretion. To investigate whether physiologic catecholamine secretion is exocytotic in humans, we measured plasma norepinephrine, epinephrine, and CgA responses to differentiated stimuli of sympathoadrenal discharge. The CgA radioimmunoassay antibody recognized authentic CgA in normal human adrenal chromaffin vesicles. Insulin-induced hypoglycemia and caffeine ingestion, in decreasing order of potency, selectively stimulated epinephrine release from the adrenal medulla. During hypoglycemia, plasma levels of epinephrine and CgA rose, and peak plasma levels of epinephrine and CgA correlated, suggesting that gradations in epinephrine release represented gradations in exocytosis. However, significant increments in plasma CgA were not observed after caffeine ingestion. Furthermore, the rise of CgA levels during hypoglycemia lagged 60 minutes behind those of epinephrine. A less-pronounced temporal dissociation between CgA and epinephrine release was also shown in isolated chromaffin cells in vitro. Selective adrenal vein catheterization suggested a barrier to CgA transport across the adrenal capillary wall. Short-term, high-intensity dynamic exercise, assumption of the upright posture, prolonged low-intensity dynamic exercise, and smoking, in decreasing order of potency, stimulated norepinephrine release from sympathetic nerve endings. Only the first sympathetic neuronal stimulus resulted in significant increments in plasma CgA, increments considerably less than those attained during adrenal medullary activation by insulin hypoglycemia. During high-intensity exercise, peak plasma norepinephrine and CgA levels correlated, suggesting that gradations in norepinephrine release represented gradations in exocytosis. The human adrenal medulla was a far more prominent tissue source of CgA than human sympathetic nerves--adrenal medullary homogenates contained 97-fold more CgA (micrograms/g) than sympathetic nerve homogenates. In conclusion, catecholamine secretion during selective stimulation of either sympathetic nerves or the adrenal medulla is, at least in part, exocytotic. Furthermore, stimulation of the former results in comparatively modest changes in plasma CgA compared with changes attained during stimulation of the latter. CgA appears to be transported by a route different from that of catecholamines from adrenal medullary chromaffin cells to the circulation in vivo.

Adrenal Glands↗
PubMed1997

Effects of cardiac denervation on development of heart failure and catecholamine desensitization.

BACKGROUND: Two signatures of heart failure are activation of the sympathetic nervous system and catecholamine desensitization. However, whether or not the elimination of cardiac nerves affects either the progression of heart failure or catecholamine desensitization is not clear. METHODS AND RESULTS: We studied 8 dogs with selective ventricular denervation (VD) (surgical technique) and 10 intact dogs, chronically instrumented for measurement of left ventricular (LV) and arterial pressures, LV dP/dt, LV internal diameter, and wall thickness before and after heart failure was induced by rapid pacing (240 bpm) for 3 to 4 weeks. VD was confirmed by the absence of reflex effects induced by intracardiac veratrine and depletion of tissue norepinephrine and by supersensitive responses to norepinephrine. During the development of heart failure, LV end-systolic and end-diastolic stresses and heart rate increased, while myocardial contractility, as reflected by LV dP/dt and mean velocity of circumferential fiber shortening corrected for heart rate (Vcf(c)), decreased in both intact and VD dogs. However, the increases in LV end-diastolic stress and decreases in LV dP/dt as well as the relationship between LV systolic stress and Vcf(c) in heart failure were less (P<.05) in VD dogs. The responses of LV dP/dt and heart rate to both isoproterenol and norepinephrine in intact dogs were reduced in heart failure. The physiological desensitization to the inotropic effects of isoproterenol and norepinephrine was less in dogs with VD (P<.05), but chronotropic responses were similar because atrial innervation remained intact. Plasma norepinephrine levels were not different in VD dogs (592+/-79 pg/mL) compared with intact dogs (576+/-81 pg/mL) in heart failure. CONCLUSIONS: Dogs with selective VD tolerated the development of heart failure better than intact dogs and demonstrated significantly less catecholamine desensitization. The latter indicates that intact ventricular innervation is required for physiological expression of catecholamine desensitization despite comparable elevation of plasma catecholamines during the development of heart failure.

Adrenergic alpha-Agonists↗
PubMed1993

In vivo hypothalamic release and synthesis of catecholamines in spontaneously hypertensive rats.

Juvenile spontaneously hypertensive rats (SHR) have higher plasma levels of catechols and markedly larger catechol responses to yohimbine than do normotensive Wistar-Kyoto rats, indicating increased sympathoadrenal outflow and increased alpha 2-adrenergic receptor-mediated restraint of peripheral catecholamine release during hypertension development in SHR. Yohimbine-induced catecholamine release and metabolism in the posterolateral hypothalamus of the brain were assessed in juvenile (6 to 7 weeks) and adult (15 to 16 weeks) SHR and Wistar-Kyoto rats. In vivo microdialysis was used to obtain samples for measurements of norepinephrine, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, and dihydroxyphenylacetic acid in conscious animals before and after yohimbine injection (1 mg/kg IV) beginning 24 hours after probe implantation. Catecholamine synthesis was examined from elevations of 3,4-dihydroxyphenylalanine levels after probe perfusion with NSD-1015, an inhibitor of L-aromatic acid decarboxylase. In adults, SHR had higher dialysate norepinephrine (277 +/- 38 versus 181 +/- 35 pg/mL), dihydroxyphenylglycol (3260 +/- 509 versus 2231 +/- 201 pg/mL), methoxyhydroxyphenylglycol (2659 +/- 369 versus 1890 +/- 144 pg/mL), and dihydroxyphenylacetic acid (46,312 +/- 5512 versus 13,187 +/- 1963 pg/mL) levels and markedly larger increases in 3,4-dihydroxyphenylalanine levels after NSD-1015 than Wistar-Kyoto rats. In juveniles, SHR had larger proportionate increments in microdialysate norepinephrine levels after yohimbine than Wistar-Kyoto rats (85% versus 25%). Although juvenile SHR and Wistar-Kyoto rats had similar NSD-1015-elicited increments in 3,4-dihydroxyphenylalanine levels, systemic yohimbine enhanced the NSD-1015-elicited 3,4-dihydroxyphenylalanine elevations in juvenile SHR but not in Wistar-Kyoto rats. These findings suggest augmented norepinephrine release and catecholamine synthesis in the posterolateral hypothalamus of adult SHR and augmented alpha 2-adrenergic receptor restraint of both norepinephrine release and catecholamine synthesis in juvenile SHR.

Aging↗
PubMedDate not supplied

Plasma catecholamines and essential hypertension. An analytical review.

Of 78 comparative studies of plasma catecholamines in patients with essential hypertension and in normotensive controls, most reported higher catecholamine levels in the hypertensives, although only about 40% of the studies were positive (reporting statistically significant hypertensive-normotensive differences). Although there was dramatic variability in catecholamine values within and across studies, virtually all studies of norepinephrine in young, consistently hypertensive patients were positive. The likelihood that a study was positive with respect to norepinephrine was independent of the likelihood with respect to epinephrine, so that total catecholamine values, or else the sum of norepinephrine plus epinephrine, differentiated hypertensives from normotensives to a greater extent than levels of either substance alone. The preponderance of literature on the subject supports the hypothesis that increased plasma catecholamine concentrations occur in some patients with essential hypertension. Elevated plasma norepinephrine in relatively young, established hypertensive patients is consistent with a pathophysiologic role for increased sympathetic neural activity in this subgroup.

Adult↗
PubMed1975

Increased plasma catecholamine concentrations and vas deferens norepinephrine biosynthesis in men with elevated blood pressure.

Systemic biochemical indexes of sympathetic nerve functionplasma catecholamine concentrations and serum dopamine-beta-hydroxylase activitywere correlated with regional indexesnorepinephrine concentration activities of norepinephrine biosynthetic enzymes in the vas deferensānd with blood pressures and pulse rates of 57 men at the time of vasectomy. Mean plasma catecholamine content was increased 66% and 60% in men with elevated systolic and elevated systolic and diastolic blood pressures, respectively. The norepinephrine concentration, tyrosine hydroxylase activity, and dopa decarboxylase activity in the vas deferens were increased in 12%, 26%, and 17% of the men with elevated blood pressure, respectively. Tyrosine hydroxylase and dopa decarboxylase in the men with elevated systolic blood pressure were increased 41% and 68%, respectively, compared with values in the men with normal blood pressure (P less than 0.05 and P less than 0.02). Individual plasma catecholamine content was related directly to both systolic and mean blood pressure (P less than 0.01) and to activities of vas deferens tyrosine hydroxylases (P less than 0.05) and dopa decarboxylase (P less than 0.01). There was a weak, but not significant, correlation of plasma catecholamine concentration with serum dopamine-beta-hydroxylase activity. Raised plasma catecholamine concentration in men with elevated blood pressure prior to vasectomy was associated with increased neurotransmitter biosynthesis in their vas deferens, which may indicate increased sympathetic nerve tonicity and perhaps be a factor contributing to the blood pressure elevation.

Adult↗
PubMed1976

Circulating catecholamine levels in human and experimental hypertension.

The radiometric enzymatic technique of Coyle and Henry (J. Neurochem. 21: 61-67, 1973) was adapted to the measurement of serum catecholamines. This technique requires less time than other enzymatic techniques and is sensitive to quantities as small as 25 pg. In normotensive subjects lying supine for 20 minutes serum catecholamine levels averaged 0.218 ng/ml, with no obvious sex or age difference. Under these standardized conditions, the circulating catecholamine levels for a given individual are highly reproducible on different days over a period of several months. In 22 patients with essential hypertension, circulating levels were significantly higher, with an average of 0.370 ng/ml. More than 50% of the hypertensive patients had values greater than the highest value measured in normotensives. Systolic blood pressure and heart rate were significantly higher in the hypertensive group with elevated levels of circulating catecholamines than in the hypertensive group with normal levels. In one model of experimental hypertension, produced in the rat by administration of deoxycorticosterone acetate (DOCA) and saline for 4-8 weeks, serum catecholamines were significantly elevated. These findings suggest that the sympathetic system may play an important role in maintaining an elevated blood pressure in experimental hypertension and in a significant proportion of patients with essential hypertension.

Animals↗
PubMedDate not supplied

Acute myocardial and plasma catecholamine changes in experimental stroke.

Focal cerebral ischemia in humans increases the incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done in 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (1/7). In animals with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre- middle cerebral artery occlusion values (+46 +/- 18% and +142 +/- 45%, respectively). As well, in cats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase in plasma concentration of norepinephrine and epinephrine. This suggests that a rise in plasma catecholamine levels, due to increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage.

Acute Disease↗
PubMed2000

Processing of chromogranin A by plasmin provides a novel mechanism for regulating catecholamine secretion.

Chromogranin A (CgA) is the major soluble protein in the core of catecholamine-storage vesicles and is also distributed widely in secretory vesicles throughout the neuroendocrine system. CgA contains the sequences for peptides that modulate catecholamine release, but the proteases responsible for the release of these bioactive peptides from CgA have not been established. We show here that the major fibrinolytic enzyme, plasmin, can cleave CgA to form a series of large fragments as well as small trichloroacetic acid-soluble peptides. Peptides generated by plasmin-mediated cleavage of CgA significantly inhibited nicotinic cholinergic stimulation of catecholamine release from PC12 cells and primary bovine adrenal chromaffin cells. We also show that the zymogen, plasminogen, as well as tissue plasminogen activator bind saturably and with high capacity to catecholaminergic (PC12) cells. Occupancy of cell surface binding sites promoted the cleavage of CgA by plasmin. Positive and negative modulation of the local cellular fibrinolytic system resulted in substantial alterations in catecholamine release. These results suggest that catecholaminergic cells express binding sites that localize fibrinolytic molecules on their surfaces to promote plasminogen activation and proteolytic processing of CgA in the environment into which CgA is secreted to generate peptides which may regulate neuroendocrine secretion. Interactions between CgA and plasmin(ogen) define a previously unrecognized autocrine/paracrine system that may have a dramatic impact upon catecholamine secretion.

Adrenal Glands↗
PubMedDate not supplied

Effects of age, feeding regimen, and glucocorticoids on catecholamine and cortisol excretion in preterm infants.

BACKGROUND: The sympathoadrenal system is important in maintaining normal physiologic functioning in infants and increased output also can reflect stress. We sought to determine the effects of age, feeding regimen, and glucocorticoids on catecholamine and cortisol excretion in preterm infants and to assess whether a particular strategy of feeding enhanced sympathoadrenal development or was stressful. METHODS: Preterm infants (26-30 wk gestation; n = 171) were assigned randomly to begin trophic feedings from day 4 through 14 (trophic group) or to start feedings at day 15 (standard group) with feedings administered either by bolus every 3 hours (bolus) or continuously over 24 hours (continuous). At 10, 28, 40, 50, and 60 days of age, urine was collected continuously for 6 hours for measurement of catecholamines (norepinephrine, epinephrine, dopamine), cortisol, and creatinine. Data were available for 98 infants. RESULTS: Norepinephrine excretion increased with postnatal age. The increase with age was significantly greater in the trophic group compared with that in the standard group. Epinephrine excretion did not change with age, and there were no differences between trophic and standard groups. Dopamine excretion increased with age but was similar between trophic and standard groups (borderline significantly greater in the trophic group). Cortisol excretion increased with age and also was similar between trophic and standard groups. There was no effect on catecholamine or cortisol excretion of bolus vs continuous feedings, antenatal or postnatal corticosteroids, gestational age at birth, age at which full feedings were attained, or use of human milk compared with preterm formula. CONCLUSIONS: The greatest determinant of catecholamine and cortisol excretion is postnatal age. Feeding method, type of feeding, and glucocorticoid administration in the amounts customarily used have little significant effect on catecholamine or cortisol excretion. The apparent link between early feeding and norepinephrine (and possibly dopamine) excretion warrants further investigation.

Age Factors↗