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At least 631 records · Page 35Linked to original sources
PubMed1983

Trifluoperazine inhibits 45Ca2+ uptake and catecholamine secretion and synthesis in adrenal medullary cells.

In isolated adrenal medullary cells, carbamylcholine and high K+ cause the calcium-dependent secretion of catecholamines with a simultaneous increase in the synthesis of 14C-catecholamines from [14C]tyrosine. In these cells, trifluoperazine, a selective antagonist of calmodulin, inhibited both the secretion and synthesis of catecholamines. The stimulatory effect of carbamylcholine was inhibited to a greater extent than that of high K+. The inhibitory effect of trifluoperazine on carbamylcholine-evoked secretion of catecholamines was not overcome by an increase in either carbamylcholine or calcium concentration, showing that inhibition by trifluoperazine occurs by a mechanism distinct from competitive antagonism at the cholinergic receptor and from direct inactivation of calcium channels. Doses of trifluoperazine that inhibited catecholamine secretion and synthesis also inhibited the uptake of radioactive calcium by the cells. These results suggest that trifluoperazine inhibits the secretion and synthesis of catecholamines mainly due to its inhibition of calcium uptake. Trifluoperazine seems to inhibit calcium uptake by uncoupling the linkage between calcium uptake by uncoupling the linkage between cholinergic receptor stimulation and calcium channel activation.

Adrenal Medulla↗
PubMed1986

Cell cycle-dependent modulation of biosynthesis and stimulus-evoked release of catecholamines in PC12 pheochromocytoma cells.

Catecholamine biosynthesis and its stimulus-evoked release in PC12 pheochromocytoma cells were studied as a function of cell cycle by means of HPLC with electrochemical detection. We found that 3,4-dihydroxyphenylethylamine (dopamine) levels in PC12 cells remained constant throughout the period of cell cycle. In contrast, the noradrenaline content was dependent on the cell cycle: it increased during the S + G2 phase followed by a decrease in the M phase. These results were confirmed further by measuring the activities catalyzing the catecholamine biosynthesis. Thus, activities of tyrosine 3-monooxygenase and 3,4-dihydroxyphenylalanine decarboxylase were independent of the cell cycle, whereas both soluble and membrane-bound dopamine beta-monooxygenase activities were modulated during the cell cycle. On the other hand, release of the catecholamines stimulated with 50 mM KCl increased in the G1 phase, reached a maximum in the late G1, and then gradually decreased in later periods. We also found that carbamylcholine-induced release of the catecholamines occurred maximally in the early S + G2 phase followed by a decrease during the M phase. Cell cycle dependence of the catecholamine release was in good agreement with that of 45Ca2+ uptake. Thus, this study provides evidence that the catecholamine biosynthesis and its release in PC12 cells are modulated during the period of cell cycle.

Animals↗
PubMed1991

Ryanodine inhibits caffeine-evoked Ca2+ mobilization and catecholamine secretion from cultured bovine adrenal chromaffin cells.

The effects of ryanodine, a selective inhibitor of the Ca(2+)-induced Ca2+ release mechanism, on caffeine-evoked changes in cytosolic Ca2+ concentration ([Ca2+]i) and catecholamine secretion were investigated using cultured bovine adrenal chromaffin cells. Caffeine (5-40 mM) caused a concentration-dependent transient rise in [Ca2+]i and catecholamine secretion in Ca2+/Mg(2+)-free medium containing 0.2 mM EGTA. Ryanodine (5 x 10(-5) M) alone had no effect on either [Ca2+]i or catecholamine secretion. Although the application of ryanodine plus caffeine caused the same increase in both [Ca2+]i and catecholamine secretion as those induced by caffeine alone, ryanodine (4 x 10(-7) - 5 x 10(-5) M) irreversibly prevented the increase in both [Ca2+]i and catecholamine secretion resulting from subsequent caffeine application over a range of concentrations. The secretory response to caffeine was markedly enhanced by replacement of Na+ with sucrose in Ca2+/Mg(2+)-free medium, and this enhanced response was also blocked by ryanodine. Caffeine was found to decrease the susceptibility of the secretory apparatus to Ca2+ in digitonin-permeabilized cells. These results indicate that caffeine mobilizes Ca2+ from intracellular stores, the function of which is irreversibly blocked by ryanodine, resulting in the increase in catecholamine secretion in the bovine adrenal chromaffin cell.

Adrenal Glands↗
PubMed1991

Adrenal medullary transplants increase spinal cord cerebrospinal fluid catecholamine levels and reduce pain sensitivity.

Previous work in this laboratory has shown that adrenal medullary transplants into the spinal cord subarachnoid space can reduce pain sensitivity. This analgesia most likely results from the release of neuroactive substances, particularly catecholamines and opioid peptides, from the transplanted cells into the CSF of the spinal cord, since it can be attenuated or blocked by alpha-adrenergic or opiate antagonists. The purpose of the present study was to more directly measure the release of catecholamines from adrenal medullary transplants in the spinal cord CSF using a spinal superfusion technique. CSF samples from rats with 6-month-old transplants were assayed for catecholamines using HPLC with electro-chemical detection. Results indicated that norepinephrine levels were increased threefold, and epinephrine levels nearly 100-fold, in animals with adrenal medullary transplants compared with control transplanted animals. There was no apparent increase in dopamine levels. Furthermore, the increased levels of total catecholamines were correlated with decreased pain sensitivity. Results of this study indicate that adrenal medullary transplants can survive for long periods in the rat spinal CSF and continue to release high levels of catecholamines. Together, the release of catecholamines and opioid peptides from adrenal medullary transplants may provide the ideal combination for the reduction of pain.

Adrenal Medulla↗
PubMed1992

Effects of handling or immobilization on plasma levels of 3,4-dihydroxyphenylalanine, catecholamines, and metabolites in rats.

In conscious animals, handling and immobilization increase plasma levels of the catecholamines norepinephrine (NE) and epinephrine (EPI). This study examined plasma concentrations of endogenous compounds related to catecholamine synthesis and metabolism during and after exposure to these stressors in conscious rats. Plasma levels of 3,4-dihydroxyphenylalanine (DOPA), NE, EPI, and dopamine (DA), the deaminated catechol metabolites 3,4-dihydroxyphenylglycol (DHPG), and 3,4-dihydroxyphenylacetic acid (DOPAC), and their O-methylated derivatives methoxyhydroxyphenylglycol (MHPG) and homovanillic acid (HVA) were measured using liquid chromatography with electrochemical detection at 1, 3, 5, 20, 60, and 120 min of immobilization. By 1 min of immobilization, plasma NE and EPI levels had already reached peak values, and plasma levels of DOPA, DHPG, DOPAC, and MHPG were increased significantly from baseline, whereas plasma DA and HVA levels were unchanged. During the remainder of the immobilization period, the increased levels of DOPA, NE, and EPI were maintained, whereas levels of the metabolites progressively increased. In animals immobilized briefly (5 min), elevated concentrations of the metabolites persisted after release from the restraint, whereas DOPA and catecholamine levels returned to baseline. Gentle handling for 1 min also significantly increased plasma levels of DOPA, NE, EPI, and the NE metabolites DHPG and MHPG, without increasing levels of DA or HVA. The results show that in conscious rats, immobilization or even gentle handling rapidly increases plasma levels of catecholamines, the catecholamine precursor DOPA, and metabolites of NE and DA, indicating rapid increases in the synthesis, release, reuptake, and metabolism of catecholamines.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Inhibitory effects of tacrine and physostigmine on catecholamine secretion and membrane currents in guinea-pig adrenal chromaffin cells.

The effects of tacrine and physostigmine on catecholamine secretion induced by veratridine and high K+, and on voltage-dependent Na+ and Ca2+ currents, were investigated in guinea-pig adrenal chromaffin cells. In perfused adrenal glands, tacrine (100 microM) caused an inhibition of veratridine-induced catecholamine secretion, but physostigmine (100 microM) did not. In dispersed cells, both tacrine (1 microM-1 mM) and physostigmine (1 microM-1 mM) decreased catecholamine secretion induced by veratridine in a dose-dependent manner. The inhibitory effect of tacrine was much greater than that of physostigmine. Tacrine alone at a high concentration (such as 1 mM) caused a substantial increase in catecholamine secretion by itself and completely abolished the veratridine-induced secretory response in dispersed cells. High-concentration physostigmine showed a similar effect, but to a much lesser extent. The high K+ (46.2 mM)-evoked catecholamine secretion from dispersed cells was not affected by tacrine (1-100 microM) or physostigmine (1 microM-1 mM). In fura-2 loaded cells, tacrine (100 microM) almost abolished [Ca2+]i rise induced by veratridine, but only slightly reduced that evoked by high K+. In voltage-clamped cells, tacrine (300 microM) depressed the voltage-dependent Na+ and Ca2+ current by about 93% and 69%, and physostigmine (300 microM) depressed them by about 30% and 17%, respectively. These results suggest that tacrine decreases the veratridine-induced catecholamine secretion primarily by inhibiting the voltage-dependent Na+ channels rather than the Ca2+ channels. Physostigmine acts in a manner similar to tacrine, but its potency is much lower than that of tacrine.

Adrenal Glands↗
PubMed1974

Role of endogenous catecholamines in the anti-inflammatory activity of alpha-adrenoceptor blocking agents.

1 Drugs which release or modify the response to catecholamines were examined for their effect on the permeability of the mouse peritoneal vascular bed to circulating plasma albumin, labelled with Evans blue.2 Phenoxybenzamine, phentolamine, piperoxane, yohimbine or cocaine reduced the extravasation of Evans blue into the peritoneum, an effect which was antagonized by beta-adrenoceptor blocking drugs. The inhibitory effect of desipramine on the extravasation of Evans blue was less completely antagonized by beta-adrenoceptor blockade.3 Inhibition of catecholamine biosynthesis, ganglion blockade or adrenergic neurone blockade antagonized the reduction in dye extravasation by alpha-adrenoceptor blocking agents and cocaine, but had no significant effect on the response to desipramine. The inhibitory effects of alpha-adrenoceptor blocking agents on dye extravasation were not prevented by bilateral adrenalectomy.4 Mice subjected to the procedure for estimation of vascular permeability excreted increased amounts of adrenaline and noradrenaline. Pretreatment with phenoxybenzamine, piperoxane or cocaine further increased catecholamine excretion, but desipramine caused only a small increase in catecholamine excretion which did not correlate with its effect on dye extravasation.5 It is suggested that phenoxybenzamine, phentolamine, piperoxane and cocaine reduce vascular permeability in the mouse peritoneum by releasing and/or potentiating the effects of endogenous catecholamines on beta-adrenoceptors. Endogenous catecholamines do not appear to be involved in the anti-inflammatory activity of desipramine.

Adrenal Glands↗
PubMed1981

Further evidence for the involvement of Na+ channels in the release of adrenal catecholamine: the effect of scorpion venom and grayanotoxin I.

1 The effects of venom from the scorpion, Leiurus quinquestriatus, and grayanotoxin I on catecholamine secretion were studied in the perfused adrenal glands of guinea-pig. 2 Scorpion venom (0.1 to 10 micrograms/ml) caused a dose-dependent increase in catecholamine output. The response to the venom was partially inhibited by atropine (0.5 mM) plus hexamethonium (1mM). The dose-response curve was shifted to the right in the presence of these blocking agents. 3 Grayanotoxin I (0.1 to 0.5 mM) caused a dose-dependent increase in catecholamine output which was significantly reduced by atropine (0.5 mM) plus hexamethonium (1 mM). However, when grayanotoxin I (0.1 mM) was applied together with scorpion venom (0.1 micrograms/ml, a concentration which alone, was almost ineffective) the maximum catecholamine output was reached even in the presence of atropine plus hexamethonium. 4 Tetrodotoxin (0.1 or 0.2 microM) reversibly inhibited the secretory response induced by scorpion venom (10 micrograms/ml) and grayanotoxin I (0.1 mM) plus scorpion venom (0.1 micrograms/ml). 5 Scorpion venom and grayanotoxin I plus scorpion venus did not cause catecholamine secretion in the absence of extracellular Na+ or Ca2+ ions. However, the secretory response was restored by reintroduction of Na+ or Ca2+ ions. 6 It is suggested that both scorpion venom and grayanotoxin I activate Na+ channels on the chromaffin cell and result in catecholamine secretion.

Adrenal Glands↗
PubMed1981

Correlation between catecholamine release and sodium pump inhibition in the perfused adrenal gland of the cat.

1 Ca(2+) reintroduction to retrogradely perfused and ouabain (10(-4) M)-treated cat adrenal glands caused a catecholamine secretory response which was greater the longer the time of exposure to the cardiac glycoside. Such a response was proportional to the external Na(+) concentration [Na(+)](o).2 A qualitatively similar, yet smaller response was observed when glands were perfused with Krebs solution lacking K(+) ions; thus, K(+) deprivation mimicked the secretory effects of ouabain. Catecholamine secretion evoked by Ca(2+) reintroduction in K(+)-free solution (0-K(+)) was also proportional to [Na(+)](o) and greater the longer the time of exposure of the gland to 0-K(+) solution.3 The ionophore X537A also mimicked the ouabain effects, since Ca(2+) reintroduction to glands treated with this agent (25 muM) caused a sharp secretory response. When added together with X537A, ouabain (10(-4) M) did not modify the response to the ionophore.4 N-ethylmaleimide (NEM), another Na(+), K(+)-ATPase inhibitor, did not evoke the release of catecholamines; on the contrary, NEM (10(-4) M) inhibited the catecholamine secretory response to high [K(+)](o), acetylcholine, Ca(2+) reintroduction and ouabain.5 Ouabain (10(-4) M) inhibited the uptake of (86)Rb into adreno-medullary tissue by 60%. Maximal inhibition had already occurred 2 min after adding the drug, indicating a lack of temporal correlation between ATPase inhibition and the ouabain secretory response, which took longer (about 30-40 min) to reach its peak. NEM (10(-4) M) blocked (86)Rb uptake in a similar manner.6 The results are further evidence in favour of the presence of a Na(+)-Ca(2+) exchange system in the chromaffin cell membrane, probably involved in the control of [Ca(2+)](i) and in the modulation of catecholamine secretion. This system is activated by increasing [Na(+)](i), either directly (ionophore X537A, increased [Na(+)](o)) or indirectly (Na(+) pump inhibition). However, the simple inhibition of Na(+) pumping does not always lead to a catecholamine secretory response; such is the case for NEM.

Adrenal Glands↗
PubMed1987

Catecholamine release evoked by lithium from the perfused adrenal gland of the cat.

The effect of Li on catecholamine release by cat isolated retrogradely perfused adrenal gland was investigated. Replacement of Na (119 mM) by Li in the Krebs solution evoked a progressive increase in the spontaneous release of catecholamines that reached a maximum within 45 min and was Ca-dependent. This response was specific for Li, since sucrose or choline used as osmotic substitutes for Na, failed to increase the spontaneous release of catecholamines by the adrenal gland. In glands perfused with Li-Krebs for 30 min a sharp secretory response was observed when Li was replaced by sucrose or choline; no such an effect was seen when Li was replaced by Na. Partial replacement of Na by sucrose, in ouabain (10(-4) M, 10 min) pretreated glands perfused with normal Krebs induced a sharp increase in the catecholamine output whilst replacement by Li produced a significantly lower response. Reintroduction of Ca (2.5 mM, 2 min) in glands previously perfused with Ca-free, Mg-containing Li-Krebs, evoked a sharp increase in catecholamine release. No such an effect was seen when the glands were perfused with Ca-free normal, choline- or sucrose-Krebs. The release of catecholamines evoked by Ca reintroduction in glands previously perfused with Ca-free Li-Krebs was directly dependent on the Li concentration and the length of time of the Li loading period. In summary, our results indicate that Li accumulates in the cells and can partially substitute Na in the Na-Ca counter-transport system at the plasma membrane of the chromaffin cell.

Adrenal Glands↗
PubMed1969

The metabolic requirements from catecholamine release from the adrenal medulla.

1. The metabolic requirements for catecholamine secretion elicited by acetylcholine or by calcium plus high K(+) were studied on acutely denervated perfused cat adrenal glands.2. Glucose-deprivation plus anoxia caused an increase in the spontaneous catecholamine output from adrenal glands perfused with normal Locke solution, which was abolished by the removal of calcium from the perfusion medium.3. Anoxia plus glucose-deprivation did not depress the secretory response to repeated exposures of a low concentration of acetylcholine, but did depress the response to a higher concentration of acetylcholine. Glucose-deprivation and nitrogen, when imposed either separately or together, did not inhibit total catecholamine output in response to calcium. Differential analysis of the calcium-evoked secretion showed that during anoxia, catecholamine output was maintained primarily by adrenaline secretion.4. Cyanide (0.2 mM) potentiated the secretory response to calcium in the presence of glucose, but when glucose was omitted from the perfusion medium, cyanide caused a gradual decline in calcium-evoked secretion. Iodoacetic acid (IAA) (0.2 mM) depressed the response to calcium by about 50% under aerobic conditions and by 90% under anaerobic conditions.5. The glycogen content of medullae was profoundly depleted under anoxic conditions.6. It is concluded that energy is required for the secretory action of calcium on medullary chromaffin cells. The energy may be derived from glycolysis or oxidative metabolism. A possible interaction between calcium and adenosine triphosphate acid (ATP) in eliciting catecholamine secretion is discussed.7. The alteration in the percent adrenaline and noradrenaline secreted during anoxia indicates that anoxia may regulate medullary catecholamine secretion through a peripheral, as well as a central mechanism.

Acetylcholine↗
PubMed1987

Vasoactive intestinal polypeptide stimulates the secretion of catecholamines from the rat adrenal gland.

1. Our previous studies have indicated that splanchnic nerves release a substance(s), other than acetylcholine, that induces the secretion of catecholamines from the rat adrenal medulla. To identify the nature of the non-cholinergic substance, the effects of met-enkephalin and vasoactive intestinal polypeptide (VIP) were investigated in the perfused adrenal gland of the rat. 2. The secretion of catecholamines increased from a basal level of 8 ng to a maximum value of 18 ng during perfusion with 100 microM-met-enkephalin. The secretion evoked by 10 micrograms acetylcholine increased from 118 to 143 ng in the presence of 10 microM-met-enkephalin. Higher concentrations of met-enkephalin (100 microM) had no additional effect. Secretion of catecholamines evoked by stimulation of splanchnic nerves (10 Hz for 30 s) was even less (8%) affected by met-enkephalin. 3. 0.3 microM-VIP caused a significant increase in the secretion of catecholamines, and the effect increased with an increase in the concentration of VIP. About 115 ng of catecholamines were secreted during 15 min perfusion with 3 microM-VIP. 4. VIP-evoked secretion was not affected by antagonists of nicotinic and muscarinic receptors, nor by chronic splanchnicotomy. However, removal of calcium ions from, and inclusion of 1 mM-EGTA in, the perfusion medium completely inhibited the secretion evoked by VIP. 5. VIP-evoked secretion was reduced (20-75%) in a concentration-dependent manner by 3-30 microM-naloxone. 6. It is suggested that VIP may be the non-cholinergic excitatory substance present in the splanchnic nerves and released along with acetylcholine during simulation of the nerves to evoke secretion of catecholamine from the rat chromaffin cells.

Acetylcholine↗
PubMed1991

The peptide VIP is a neurotransmitter in rat adrenal medulla: physiological role in controlling catecholamine secretion.

1. The perfused adrenal gland of the rat was used to establish the identity of a non-cholinergic substance involved in splanchnic nerve-mediated secretion of catecholamines. 2. The perfused adrenal medulla was rich in vasoactive intestinal polypeptide (VIP) content (28 pmol g-1 of wet tissue). VIP-immunoreactive nerve fibres were present in the adrenal medulla and the adrenal cortex. 3. Field stimulation (10 Hz for 15 min plus 1 Hz for 15 min) caused a large increase in the output of VIP in the perfusate over the spontaneous release of VIP. Secretion of catecholamines was also greatly elevated by field stimulation. Field stimulation-evoked output of VIP and catecholamines was abolished after chronic denervation of the adrenal glands. 4. Infusion of acetylcholine (ACh) did not increase the output of VIP but caused a robust secretion of catecholamines. 5. The VIP output declined when the stimulation frequency was increased (8.6 x 10(-3) fmol pulse-1 at 1 Hz and 4.0 x 10(-3) fmol pulse-1 at 10 Hz). 6. In contrast, the output of 3H-acetylcholine (3H-ACh, expressed as a fraction of tissue 3H-ACh content) increased from 7.0 x 10(-2) pulse-1 at 1 Hz to 16.3 x 10(-2) pulse-1 at 10 Hz. 7. Secretion of catecholamines evoked by low-frequency stimulation (1 Hz) was reduced by 40% in the presence of cholinergic receptor antagonists (atropine plus hexamethonium). Inclusion of a VIP receptor antagonist ([Ac-Tyr1, D-Phe2]-GRF 1-29 amide) caused about 75% inhibition. 8. The VIP receptor antagonist inhibited VIP-evoked secretion of catecholamines without affecting ACh-evoked secretion. 9. In conclusion, VIP satisfies all the essential criteria to assume the role of a neurotransmitter in the rat adrenal medulla. The contribution of VIP to the secretion of adrenal medullary hormones is more prominent at low rates of neuronal activity whereas ACh is the major contributor at higher activity.

Acetylcholine↗
PubMed1994

Developmental changes in hypoxia-induced catecholamine release from rat carotid body, in vitro.

1. Developmental changes in free tissue catecholamine levels were studied using Nafion-coated, carbon fibre electrodes placed in rat carotid bodies, in vitro. Simultaneously, single fibre chemoreceptor afferent activity was recorded from the sinus nerve. Five age groups were examined: 1, 2, 6, 10 and 20-30 days of age. 2. Using fast-scan voltammetry, similar current peaks were observed during exposure to exogenous dopamine and during superfusion with hypoxic saline. This suggests that changes in carbon fibre electrode current are due to an increase in free tissue catecholamines. 3. Baseline catecholamine levels were significantly less in the 1-6 day age groups compared to 10 day and 20-30 day rats. 4. During 1 min of hypoxia the peak concentration of tissue catecholamine was significantly less in the 1 day compared to the 2 day age groups, and these were less than in 10 day and 20-30 day rats. 5. Peak nerve response during hypoxia increased with age from 4.5 +/- 0.6 Hz in the 1 day to 10.5 +/- 1.6 Hz in the 6 day and to 15.5 +/- 2.2 Hz in the 20-30 day rats. 6. We conclude that (1) resting free tissue catecholamine levels increase with age in the newborn period, (2) hypoxia causes enhanced catecholamine release, and (3) the magnitude of the release increases in the postnatal period as does the nerve activity.

Afferent Pathways↗
PubMed1996

Plasma catecholamines and hyperglycaemia influence thermoregulation in man during prolonged exercise in the heat.

1. We manipulated plasma catecholamines (combined adrenaline and noradrenaline concentrations) to three levels during prolonged exercise to determine their effect on cutaneous and forearm vascular conductance (CVC and FVC), oesophageal temperature (T(oes)) and cardiovascular responses. 2. On three occasions, seven endurance-trained men cycled at 65% VO2, max in the heat (33.1 +/- 0.7 degrees C) for 120-150 min. During the control trial (150 min duration), 0.45% saline was intravenously infused (SI) starting at 30 min, at a rate that replaced a third of the fluid losses. The infusion start time and rate were identical in all three trials. During SI, plasma catecholamine levels increased progressively and were 18.2 +/- 2.7 pmol ml-1 at 150 min. In another trial (120 min duration), adrenaline was infused (AI) at 0.1 microgram kg-1 min-1 and plasma catecholamine levels were elevated 6 pmol ml-1 above SI during the 60-120 min period. In a third trial (150 min duration), an 18% glucose solution was infused (GI) at a rate that maintained plasma glucose levels above 11 mM and plasma catecholamine levels were 5.0-5.5 pmol ml-1 lower (P < 0.05) than SI from 120-150 min. 3. Heat production and sweat rate were not different during the three trials and neither was the decline in stroke volume, cardiac output and mean arterial pressure. 4. Soon after beginning AI, CVC decreased 15%, T(oes) increased by 0.4 +/- 0.1 degree C and heart rate increased by 6 +/- 1 beats min-1; these significant (P < 0.05) differences from SI were maintained throughout the bout. As a result of GI, FVC was 15% higher than SI and T(oes) and heart rate were attenuated by 0.3 +/- 0.1 degree C and 7 +/- 1 beats min-1 at 150 min compared with SI (P < 0.05). 5. In conclusion, large increases in plasma catecholamine levels cause hyperthermia during exercise by vasoconstricting the skin. The mechanisms by which hyperglycaemia (i.e. 11 mM) attenuates hyperthermia are less clear and may be due to others factors besides attenuation of the plasma catecholamine response to exercise.

Adult↗
PubMed2002

Prognostic implications of autonomic function assessed by analyses of catecholamines and heart rate variability in stable angina pectoris.

OBJECTIVE: To assess the prognostic impact of autonomic activity, as reflected by catecholamines and heart rate variability (HRV), in patients with stable angina pectoris. DESIGN: Double blind, randomised treatment with metoprolol or verapamil. 24 hour ambulatory ECG, used for frequency domain analyses of HRV, and symptom limited exercise tests at baseline and after one month of treatment. Catecholamine concentrations were measured in plasma (rest and exercise) and urine. SETTING: Single centre at a university hospital. PATIENTS: 641 patients (449 men) with stable angina pectoris. MAIN OUTCOME MEASURES: Cardiovascular (CV) death, non-fatal myocardial infarction (MI). RESULTS: During follow up (median 40 months) there were 27 CV deaths and 26 MIs. Patients who died of CV causes had lower total power and high (HF), low (LF), and very low (VLF) frequency components of HRV. HRV was not altered in patients who suffered non-fatal MI. Catecholamines did not differ between patients with and those without events. Metoprolol increased HRV. Verapamil decreased noradrenaline (norepinephrine) excretion. Multivariate Cox analyses showed that total power, HF, LF, and VLF independently predicted CV death (also non-sudden death) but not MI. LF:HF ratios and catecholamines were not related to prognosis. Treatment effects on HRV did not influence prognosis. CONCLUSIONS: Low HRV predicted CV death but not non-fatal MI. Neither the LF:HF ratio nor catecholamines carried any prognostic information. Metoprolol and verapamil influenced LF, HF, and catecholamines differently but treatment effects were not related to prognosis.

Adult↗
PubMed2003

[Catecholamine response to the Wingate test in untrained women].

Supramaximal exercises are well known to induce a severe stress on the adrenal medulla and nervous sympathetic system. This stress induces increased plasma catecholamines concentrations. The responses of catecholamines to supramaximal exercises in women are still not well characterized and have been studied mostly in trained subjects. Hence the aim of the present study was to evaluate plasma catecholamine responses to a Wingate test in young and untrained women (n = 6) and men (n = 7). Venous plasma catecholamine concentrations were determined by HPLC, at rest, at the end of the warm-up and of the exercise, and during recovery (5, 10, 20, and 30 mn). Our results failed to show any significant difference in resting catecholamine concentrations ([A]p: 0.41 +/- 0.05 vs. 0.45 +/- 0.05 nmol. L-1; [NA]p: 3.28 +/- 0.68 vs. 2.58 +/- 0.26 nmol.L-1), kinetics, and maximal plasma catecholamine concentrations (Amax: 4.47 +/- 1.08 vs. 3.31 +/- 0.63 nmol.L-1; NAmax: 18.05 +/- 1.11 vs. 14.01 +/- 2.02 nmol.L-1) in response to the Wingate test between women and men, respectively. The Amax/NAmax ratio used as an index of adrenal medulla sensitivity to sympathetic input was also similar between genders. In conclusion, this study was able to demonstrate, in untrained subjects, that gender did not alder the sympatho-adrenergic response induced by a severe stress.

Adolescent↗
PubMed1977

Effect of acute stress and ouabain administration on adrenal catecholamine content and cardiac function of rats pretreated with diazepam.

The experiments described were carried out in an attempt to determine the participation of adrenal catecholamines in the higher incidence of cardiac arrhythmias produced by acute stress or ouabain injections in diazepam-treated animals. The pretreatments of rats with diazepam (150 mg kg-1 d-1) increase significantly the adrenal catecholamine content. Consequently, the application of electrical and immobilization stress releases more catecholamines from the adrenal glands of the diazepam-treated rats and also produces higher incidence of ventricular extrasystoles. Furthermore, various pretreatments of rats with diazepam (5-150 mg kg-1 d-1) also lead to an increase in the catecholamine content of the adrenal gland. In diazepam-treated rats, the intravenous administration of ouabain produces a greater release of adrenal catecholamines as well as a greater incidence of cardiac arrhythmias. Several hypotheses are proposed to explain the elevation of adrenal catecholamines and also the higher incidence of ventricular arrhythmias.

Adrenal Glands↗