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PubMed1989

The key role of sodium in the ouabain-mediated potentiation of potassium-evoked catecholamine release in cat adrenal glands.

1. The effect of [Na]o on the catecholamine release evoked by K in ouabain pretreated, isolated adrenal glands of the cat, was investigated. 2. Reduction of [Na]o to 70, 50 and 25 mM, with sucrose as a substitute, did not modify the spontaneous catecholamine release but progressively increased the K (17.7 mM)-evoked secretory response. 3. Ouabain pretreatment (100 microM; 10 min) greatly increased the K (17.7 mM)-evoked catecholamine secretory response in glands perfused with normal Krebs. Such an increase was still seen in glands perfused with 70 mM Na-containing solution but disappeared when [Na]o was reduced to 25 and 10 mM. 4. Preperfusion of non-ouabain treated glands with Li-enriched Krebs, for a 40 min period, caused an increase in the K (17.7 mM)-evoked secretory response which was dependent on [Li]o and essentially similar to that induced by ouabain pretreatment. 5. Ouabain treatment (100 microM; 10 min) of glands perfused with normal Krebs evoked a long lasting catecholamine release, which reached a plateau at about 36 min and amounted to 0.68 +/- 0.25 microgram 2 min-1 (n = 9). Such a secretory response was dramatically increased, and its shape modified, when glands were preperfused with K (17.7 mM)-Krebs: a peak of 3.77 +/- 0.42 micrograms 2 min-1 (n = 7) was reached at 18 min. This response was drastically reduced in the presence of nitrendipine (1 microM). 6. In summary, our results indicate that both [Na]0 reduction or Na accumulation into the chromaffin cell by inhibition of the Na pump with ouabain, greatly enhance the secretory efficacy of small increments of [K]0, and suggest that sodium may play a role in the regulation of catecholamine release mediated by voltage-dependent Ca channels in adrenal glands.

Adrenal Glands↗
PubMed1990

The role of Na+ in muscarinic receptor-mediated catecholamine secretion in the absence of extracellular Ca2+ in cat perfused adrenal glands.

1. The role of Na+ in muscarinic receptor-mediated catecholamine secretion, which is independent of extracellular Ca2+, was investigated by observing the effect of veratridine and ouabain in perfused adrenal glands of the cat. 2. Veratridine (10(-4) M) markedly enhanced catecholamine secretion evoked by acetylcholine (ACh, 10(-4) M) during perfusion with Ca2(+)-free Locke solution containing hexamethonium (10(-3) M). The enhancement tended to be larger for noradrenaline secretion than for adrenaline secretion. Qualitatively the same result was obtained in the response to pilocarpine (5 x 10(-4) M). 3. Ouabain (10(-4) M) also enhanced ACh- and pilocarpine-induced catecholamine secretions, especially noradrenaline secretion in the absence of extracellular Ca2+. 4. Tetrodotoxin (10(-6) M) blocked the enhancing effect of veratridine on ACh-induced catecholamine secretion, but not that of ouabain in the absence of extracellular Ca2+. 5. When NaCl was replaced with sucrose, there was no secretory response to ACh regardless of the presence or absence of veratridine or ouabain. However, when ouabain, but not veratridine, was infused with Na+ before the replacement of NaCl, the response to ACh was substantially augmented. 6. These results indicate that Na+ is essential in the initiation of muscarinic receptor-mediated catecholamine secretion and its enhancement by veratridine and ouabain in the absence of extracellular Ca2+. Both drugs seem to increase the intracellular concentration of Na+ through different mechanisms and result in increases in the efficiency of Ca2+ mobilization from intracellular Ca2+ pools linked to muscarinic receptors.

Acetylcholine↗
PubMed1984

Catecholamine stimulation of copper dependent haemolysis: protective action of superoxide dismutase, catalase, hydroxyl radical scavengers and serum proteins (ceruloplasmin, albumin and apotransferrin).

Copper induced lysis of washed rat erythrocytes was stimulated by catecholamines, the order of effectiveness being: adrenaline greater than noradrenaline approximately equal to dopamine greater than L-DOPA. The degree of effectiveness is related to the rate of copper ion dependent oxidation of catecholamine, adrenaline being more rapidly oxidized than the other catecholamines investigated. Superoxide dismutase, catalase and different hydroxyl radical scavengers (mannitol, tris, formate and ethanol) markedly reduced the haemolytic effect of copper and catecholamine, suggesting the possibility that superoxide radicals and hydrogen peroxide, formed in the reaction system, cooperate in producing hydroxyl radicals, which are directly involved in the haemolytic action. The plasma proteins, ceruloplasmin, albumin and apotransferrin, also reduced the copper-catecholamine induced haemolysis. The protective action is probably not related to the copper binding ability of these proteins.

Animals↗
PubMed2002

Regulation of catecholamine synthesis by leptin.

Obesity is often associated with cardiovascular and metabolic disorders such as hypertension and hyperglycemia. Leptin, a protein product of the obese gene, regulates satiety and energy expenditure through its receptors in the hypothalamus. Recent studies have shown that leptin has extrahypothalamic and peripheral actions. The presence of leptin receptors has been reported in the adrenal medulla. In the present study, we examined the effects of leptin on catecholamine synthesis in cultured bovine adrenal medullary cells. Leptin (3-30 nM) caused a significant increase in (14)C-catecholamine synthesis from [(14)C] tyrosine, but not from [(14)C] DOPA. Incubation of cells with leptin resulted in an activation and phosphorylation of tyrosine hydroxylase. Leptin caused a transient activation of mitogen-activated protein kinases (MAPKs). U0126, an inhibitor of MAPK kinase, abolished the effect of leptin on (14)C-catecholamine synthesis. High concentrations of leptin (10-100 nM) produced an increase in intracellular Ca(2+) concentration, which was blocked by Cd(2+), an inhibitor of voltage-dependent Ca(2+) channels. Concurrent treatment of cells with leptin (10 nM) and acetylcholine (0.3 mM) potently enhanced the stimulatory effect of acetylcholine on (14)C-catecholamine synthesis. Leptin, however, failed to enhance the stimulatory effect of acetylcholine on the phosphorylation and activity of tyrosine hydroxylase. Acetylcholine (0.3 mM) decreased the intracellular pH (pHi). Leptin (10 nM) affected neither the basal pHi nor the acetylcholine-induced fall in pHi. These findings suggest that leptin phosphorylates and activates tyrosine hydroxylase and subsequently stimulates catecholamine synthesis through MAPK and probably Ca(2+) pathways in the adrenal medulla.

Adrenal Medulla↗
PubMed1975

A calcium ionophore stimulating the secretion of catecholamines from the cat adrenal.

1. Experiments were performed on perfused cat adrenal glands to examine the effect of a calcium ionophore A-23187 in the secretion of catecholamines. 2. Ionophore (1-10 muM) caused a dose-dependent release of catecholamines and the output was about 100-fold greater at 10 mum than at 1 mum. 3. Release of catecholamines by the ionophore was dependent on the calcium concentration of the perfusion medium. Omission of calcium blocked the response to the ionophore while excess calcium facilitated it. 4. Magnesium antagonized the secretory response to the ionophore. Excess calcium overcame the inhibitory effect of magnesium. 5. The ionophore did not modify release of catecholamines by induced splanchnic nerve stimulation. 6. The results suggest that the ionophore, like depolarization, introduces calcium into the chromaffin cell to cause release of catecholamines.

Adrenal Glands↗
PubMed1975

Plasma catecholamines in foetal and adult sheep.

1. Foetal and maternal plasma catecholamine concentrations were measured during and after hypoxia (mean maternal Pa,02 44mmHg) in chronically catheterized sheep, 118-141 days pregnant. 2. In most foetuses the initial plasma catecholamines were smaller than 0.07 ng/ml. During hypoxia plasma adrenaline and noradrenaline always rose; there was a rise in arterial pressure and a fall in heart rate. 3. The initial catecholamine concentration in the ewes was smaller than 0.05-2.3 ng/ml. During hypoxia there was no consistent change; the maternal plasma concentrations were less than the foetal. 4. Infusion of adrenaline at 0.3 mug kg(-1) min(-1) to the ewe resulted in plasma catecholamine concentrations higher than those observed during hypoxia. There was a rise in heart rate but no consistent change in arterial pressure. 5. Infusion of adrenaline 0.4 mug kg(-1) min(-1) into the foetal jugular vein caused a rise in plasma concentration similar to that seen during hypoxia. There was a rise in heart rate but no significant change in arterial pressure. 6. The half-life of adrenaline and of noradrenaline in the maternal and foetal circulation was 0.25-1 min. There was no evidence of transfer of labelled catecholamine across the placenta.

Animals↗
PubMed1975

Catecholamine release from bovine adrenal medulla in response to maintained depolarization.

Prolonged exposure of venous-perfused bovine adrenal glands to high K in the presence of external Ca produces a transient increase in catecholamine output that reaches a maximum after about 1 min and then declines with a half-time of about 1-2 min. 2. The time course of the transient secretory response to high K does not depend appreciably on the total catecholamine output which indicates that depletion of releasable catecholamine is unlikely to be responsible for the transient nature of the response. 3. Application of 3-6 mM-Ba stimulates secretion from a gland after many minutes exposure to high K, when catecholamine output has declined close to resting levels. This provides further evidence that depletion does not play a major role in the transient response and shows that maintained depolarization does not inhibit the secretory mechanism. 4. Exposure to high K solutions in which Ca has been replaced isomotically by Mg does not evoke any catecholamine output. Subsequent application of Ca always elicits some secretion although the size of this response to added Ca declines rapidly during exposure to Ca-free, high K solutions. The failure of the secretory response in these experiments is more rapid, and earlier in onset than the declining phase of the normal secretory response evoked in the presence of calcium. 5. Pre-treatment with Ca-free solutions of intermediate K content reduces the response to subsequent simultaneous application of high K and Ca. There is a roughly sigmoidal relation between the reduction in response and the logarithm of the K concentration used for pre-treatment. 6. Thin slices of bovine adrenal medulla show qualitatively similar responses on exposure to high K. Examination of the flourescent signal from slices dyed with the potential-sensitive dye DiS-C(3)-(5) suggests that maintained exposure to high K produces a stable depolarization. 7. The most likely explanation for these results is that K-depolarization first activates and subsequently inactivates a potential-sensitive Ca permeability channel. This inactivation is time and possibly potential dependent. 8. The effect of high K on calcium movements in medullary slices was examined. Exposure to 72 mM-K increases (45)Ca uptake, the increase being greatest during the first 10 min. The efflux of Ca is also increased on exposure to high K in the presence of Ca. The net Ca uptake in 72 mM-K is smaller than the tracer uptake of Ca. These findings indicate that K depolarization stimulates a Ca-Ca exchange process. They are also consistent with, but do not offer strong positive support for, the idea that K-depolarization first activates and subsequently inactivates Ca entry. 9. It is suggested that Ca inactivation might play a role in the modulation of neurosecretion and neurotransmitter release by changes in membrane potential.

Adrenal Medulla↗
PubMed1987

Catecholamines release mediators in the opossum oesophageal circular smooth muscle.

1. Effects of catecholamines applied exogenously to the circular smooth muscle layer of the body of the oesophagus of the opossum (Didelphis marsupialis) were studied, simultaneously measuring changes in the membrane potential, the membrane conductance and the contractility of the muscle, using the double sucrose-gap technique. 2. Superfusion of the smooth muscle with Krebs solution at 27 degrees C containing dopamine (10(-6)-10(-4) M) dose-dependently caused a hyperpolarization of the smooth muscle cells and an increased membrane resistance followed after gradual repolarization by oscillations of the membrane potential, often accompanied by muscle action potentials. During the hyperpolarization, the tendency for the membrane potential to sag during prolonged application of hyperpolarizing currents was reduced and the 'off' depolarization following such currents was increased. This muscle did not develop active tension prior to treatment; it therefore did not relax during the hyperpolarizations, but contracted following the depolarized phase of oscillations. 3. The non-adrenergic, non-cholinergic nerve-mediated inhibitory junction potential (i.j.p.) showed a small reduction in amplitude during superfusion with dopamine, explicable as a result of the drug-induced hyperpolarization. The 'off' response following the i.j.p., decreased transiently when the membrane potential was hyperpolarized to its maximum value. Then it increased to values larger than control as the membrane repolarized. Vasoactive intestinal polypeptide (VIP, 10(-6) M) produced a similar response but hyperpolarizations were smaller. 4. Of the tested catecholamines, isoprenaline, phenylephrine, butylated hydroxytoluene-920 (BHT-920) and clonidine were ineffective whereas the potency order for other catecholamines was dopamine greater than noradrenaline greater than or equal to adrenaline greater than DOPA. The catecholamine-induced responses were not affected by alpha- or beta-adrenoreceptor antagonists given alone or in combination. Of the dopamine receptor antagonists tested domperidone was without effect, whereas haloperidol reduced and bulbocapnine blocked the response. The findings suggested that a receptor resembling DA1-type peripheral receptor mediated the effects of dopamine on opossum oesophagus. 5. The catecholamine-induced responses and those to VIP disappeared completely in Cl-(-)free medium (isethionate replacement). 6. Conditioning depolarization of the smooth muscle cells decreased but hyperpolarization increased the amplitude of the hyperpolarization (up to 20 mV). With larger hyperpolarizations the responses decreased and disappeared at around 50 mV hyperpolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1980

Brainstem catecholamine neurons are target sites for sex steroid hormones.

Sex steroid hormones and catecholamines have physiological interactions in the brain. By the combined use of autoradiography and fluorescence histochemistry, steroid hormone target sites and catecholamine neurons were visualized simultaneously in the same tissue preparation. By this dual localization method, [3H]estradiol and [3H]dihydrotestosterone target sites were identified in nuclei of many catecholamine cell bodies in the brainstem, and catecholamine nerve terminals were observed near certain steroid hormone target neurons. These results suggest close anatomical interrelations between steroid hormone sites of action and catecholamine sites of production and action in the brain.

Adrenalectomy↗
PubMed1990

Catecholamines and virulence of Cryptococcus neoformans.

Cryptococcus neoformans was unable to utilize catecholamines (epinephrine, norepinephrine, or dopamine) as sole carbon or nitrogen sources. Therefore, catecholamines are not essential growth factors for this fungus and the brain is not a preferred nutritional niche for its growth with regard to catecholamines. To establish whether the brain is a survival niche for C. neoformans and to explain the role of phenoloxidase as a virulence factor, a wild-type strain that had phenoloxidase activity and mutants which lacked it were exposed to an epinephrine oxidative system, and the survival of both strains was tested. The oxidative system contained epinephrine as an electron donor, Fe3+ as the catalytic transition metal ion, and hydrogen peroxide as an electron acceptor. The wild-type strain was found to be resistant to this oxidative system, whereas under the same conditions the mutant strain was susceptible and its survival decreased at a rate of 4 logs per h. Damage to high-molecular-weight DNA seems to be a causative factor of cell death after exposure of the mutants to the oxidative system. These results suggest that C. neoformans may survive in the brain because of its ability to utilize catecholamines for melanogenesis and thus neutralize the harmful effects of catecholamines which are manifested in the presence of hydrogen peroxide and transition metal ions. The role of phenoloxidase in resistance to the epinephrine oxidative system is also discussed.

Catechol Oxidase↗
PubMed1977

Increased circulating plasma catecholamines and plasma renin activity in dogs after chemical sympathectomy with 6-hydroxydopamine.

Circulating plasma catecholamines, plasma renin activity, and other variables were measured in unanesthetized dogs before and after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 50 mg/kg). Chemical sympathectomy resulted in an immediate fall in mean arterial blood pressure and a delayed reduction in heart rate. Significant increases in plasma glucose and lactate concentrations, circulating plasma catecholamines, and plasma renin activity were found 24 h after 6-OHDA treatment. Circulating catecholamine levels decreased rapidly as time elapsed after sympathectomy and were half the initial values after 2 weeks. Plasma renin activity remained elevated during the 1st week after 6-OHDA treatment and returned to control levels during the 2nd week. Significant correlations were found between circulating catecholamines and heart rate mean arterial pressure, and plasma glucose and lactate concentrations. A significant correlation was also found between plasma renin activity and the mean arterial blood pressure. These results confirm that the adrenal medulla increases its catecholamine secretion rate into the circulation to compensate for the loss of adrenergic innervation after 6-OHDA treatment. They also indicate that the renin-angiotensin system represents another important compensatory mechanism for circulatory homeostasis in sympathectomized animals.

Animals↗
PubMed1991

Modulation by beta-adrenoceptors and angiotensin II receptors of splanchnic nerve evoked catecholamine release from the adrenal medulla.

In the present study, we have evaluated the effect of both facilitatory beta 2-adrenoceptor and angiotensin II receptor on the release of adrenal catecholamines induced by electrical stimulation of the splanchnic nerve in anaesthetized and vagotomized dog. In these experiments, individual or combined treatments with the beta 2-adrenoceptor antagonist ICI 118551 (0.3 mg/kg i.v.), the converting enzyme inhibitor captopril (2 mg/kg i.v.), or the angiotensin II receptor antagonist saralasin (2 micrograms.kg-1.min-1 i.v.) were found to significantly decrease the release of adrenal catecholamines during splanchnic nerve stimulation (5-V pulses of 2 ms duration for 3 min at 1 Hz) whatever the order of administration of the drugs. On the other hand, the infusion of angiotensin II (20 ng.kg-1.min-1) was shown to potentiate the release of adrenal catecholamines in response to electrical stimulation, and this effect was totally blocked by treatment with saralasin (4 micrograms.kg-1.min-1 i.v.). This facilitating angiotensin mechanism differed from beta-adrenoceptor facilitating mechanism, since following beta-blockade with ICI 118551, angiotensin II infusion still significantly potentiated the release of catecholamines during splanchnic nerve stimulation. These observations thus suggest that both facilitating beta 2-adrenoceptors and angiotensin II receptors can independently modulate the release of adrenal catecholamines.

Adrenal Medulla↗
PubMed1992

Effects of Na-K-ATPase inhibition on catecholamine reactivity in rat pulmonary artery.

The objective of this study was to determine the effects of Na-K-adenosinetriphosphatase (ATPase) inhibition on aspects of vascular reactivity in rat pulmonary artery, including resting tone and catecholamine reactivity, loss of reactivity to repeated catecholamine stimulation, and contraction-relaxation kinetics. The effect of ATPase inhibition on resting tone and catecholamine reactivity was determined by comparing the responses to 10(-4) and 10(-3) M ouabain (Oua-4, Oua-3), 10(-4) M tyramine, and 10(-6) M norepinephrine (NE) pre- and postouabain. Loss of responsiveness to NE was induced by repeated cumulative doses of NE (NE I, NE II) with 60 min between exposures. ATPase inhibition was superimposed on this loss of reactivity by 1) administration of Oua-4 or Oua-3 15 min before NE II, 2) incubation in K(+)-free solution 15 min before NE II, and 3) incubation in K(+)-free solution 15 min before NE I for the entire protocol. The effect of ATPase inhibition on the response pattern after repetitive dosing with phenylephrine (PE) and KCl was also determined. To correlate ATPase activity with the loss of reactivity after catecholamine stimulation, we measured ATPase activity (86Rb uptake) at different time points after repeated NE administration. The effect of ATPase inhibition on contraction-relaxation rates after catecholamine stimulation was determined by analyzing the response to repeated single doses of NE in normal salt solution and after incubation in K(+)-free solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Effects of catecholamines on myocardial endogenous substrates and contractility.

The effects of epinephrine and norepinephrine on triglyceride and glycogen metabolism and contractility were studied in isolated perfused working rat hearts. Hearts with lipids prelabeled in vivo with [1-14C]palmitate were perfused with bicarbonate buffer containing 5.5 mM glucose, with or without 0.6 mM palmitate (3% albumin), and varying concentrations of catecholamines. Direct evidence for catecholamine-stimulated myocardial triglyceride lipolysis was obtained and, for the first time, was shown to be concentration-dependent. Also, catecholamines enhanced heart triglyceride fatty acid oxidation in concentration-dependent fashion. Stimulation of lipolysis and oxidation was observed only in hearts perfused with buffer containing glucose as the sole substrate, and was inhibited in the presence of 0.6 mM palmitate. Palmitate inhibited net glycogenolysis in the absence of catecholamines, but had little effect on epinephrine-stimulated glycogenolysis. Therefore, with free fatty acids present, mobilization of endogenous triglycerides to meet the increased metabolic demands of catecholamine stimulation is minimized; this is due, possibly, to enhanced utilization of exogenous free fatty acids and to inhibition of net lipolysis.

Animals↗
PubMed1994

Maturation of catecholamine response and extraneuronal uptake in rabbit trachea.

The present study investigated whether maturational changes in extraneuronal catecholamine clearance accounted for the ontogenetic attenuation of isoproterenol responsiveness in rabbit tracheal segments. Following half-maximal contraction with acetylcholine (ACh) or KCl, tracheal ring segments (TS) isolated from newborn, 1-mo, and adult rabbits were relaxed with cumulative administration of isoproterenol. With postnatal maturation, there occurred a significant decrease in both maximal relaxation and sensitivity to isoproterenol in both ACh- and KCl-contracted TS. Inhibition of extraneuronal catecholamine uptake with methylprednisolone resulted in enhanced sensitivity to isoproterenol in 1-mo and adult, but not in newborn tracheal segments. In separate studies, extraneuronal catecholamine uptake was directly assayed in tracheal segments isolated from rabbits of similar age and pretreated with neuronal uptake and monoamine oxidase inhibitors. Maximal extraneuronal uptake of [3H]norepinephrine significantly decreased with age in tracheal tissues. In contrast, the sensitivity of the uptake process to norepinephrine increased with age. The relative catecholamine reserve markedly decreased with age in rabbit tracheal segments and was directly related to the maximal degree of relaxation elicited with the beta-adrenergic catecholamine, isoproterenol, in age-matched TS precontracted with either ACh or KCl. These findings suggest that, with maturation, extraneuronal uptake more effectively competes with beta-adrenoreceptor stimulation and, accordingly, may contribute to the ontogenetic attenuation of beta-adrenergic responsiveness in rabbit tracheal tissues.

Aging↗
PubMed2006

Hypotensive hypovolemia and hypoglycemia activate different hindbrain catecholamine neurons with projections to the hypothalamus.

To better understand the involvement of hindbrain catecholamine neurons in hypovolemia-induced secretion of AVP, we injected antidopamine beta-hydroxylase saporin (DSAP) or unconjugated saporin (SAP) control solution into the hypothalamic paraventricular nucleus (PVH) of anesthetized rats to retrogradely lesion catecholamine neurons innervating magnocellular areas of the hypothalamus. Subsequently, hypotensive hypovolemia was induced by remote blood withdrawal (4.5 ml, 1 ml/min) using an intra-atrial catheter. Blood was sampled at 2, 5, 20, and 50 min after onset of blood withdrawal. The AVP response was severely impaired by DSAP. Peak responses at 50 min were 51 pg/ml in SAP control and 17 pg/ml in DSAP-lesioned rats, indicating the importance of catecholamine neurons for this response. We also measured AVP responses to osmotic challenge induced by administration of hypertonic saline (1 M, 15 ml/kg, sc) and to insulin-induced hypoglycemia. Osmotic challenge increased AVP levels, but the response was not impaired by DSAP, indicating that AVP neurons were not damaged by the DSAP injection. Insulin-induced hypoglycemia did not increase AVP levels in either DSAP- or SAP-treated rats. However, the same dose of insulin increased food intake and corticosterone secretion in SAP controls, and these responses were profoundly impaired by DSAP. Thus catecholamine neurons are required for both the AVP response to hypotensive hypovolemia and for feeding and corticosterone responses to hypoglycemia. Lack of an AVP response to insulin-induced hypoglycemia in intact rats therefore indicates that responses to hypovolemia and hypoglycemia are mediated by different catecholamine neurons under distinct sensory controls.

Animals↗
PubMed1986

Effect of hypoxemia on plasma catecholamines in intact and immunosympathectomized fetal lambs.

Fetal lambs treated with sheep anti-mouse nerve growth factor antibodies (anti-NGF) at 80 days gestation subsequently showed a diminished cardiovascular response to intravenous infusion of tyramine (1 mg/min over 10 min) and no significant change in plasma norepinephrine concentrations as measured by reversed-phase high-pressure liquid chromatography and electrochemical detection. At autopsy at 135 days gestation, catecholamine content of the heart, thyroid, kidney, and ileum was reduced by greater than 70% compared with age-matched control fetuses. The anti-NGF-treated fetuses were thus judged to have impaired sympathetic function. When made hypoxemic (arterial PO2 12-14 Torr) for 1 h at 120 or 130 days gestation, anti-NGF-treated fetuses showed no significant change of arterial pressure, heart rate, or plasma catecholamines, whereas control fetuses showed bradycardia, a 28% increase in arterial pressure, and a 670% increase of plasma norepinephrine concentrations. These results suggest that the increase of arterial pressure that occurs during hypoxemia in fetal lambs between 120 and 135 days gestation is attributable to increased activity of the peripheral sympathetic nervous system. The adrenal medulla appears to contribute to the plasma catecholamine pool at rest, but the lack of increased plasma catecholamines during hypoxia after anti-NGF implies that the adrenal medulla was unable to release catecholamines. Possible reasons for this are discussed.

Animals↗
PubMed1989

Effects of anoxia on catecholamine levels in brain and kidney of the crucian carp.

Catecholamine synthesis requires O2. Crucian carp (Carassius carassius L.), which are extremely anoxia tolerant, were exposed to anoxia for 76 or 160 h. The brain levels of dopamine and norepinephrine (no epinephrine was found in brain) remained relatively constant even after nearly 1 wk of anoxia, indicating very well-functioning transmitter reuptake mechanisms and/or the absence of O2-independent degradation. In contrast, in the kidney (which contains chromaffin tissue), the catecholamine content (at least norepinephrine) decreased by 22-60% after 160 h of anoxia. Moreover, when anoxic crucian carps were put in normoxic water for approximately 40 min, the kidney catecholamine levels increased by 50-370%, whereas no significant effect was seen in brain. Thus, in the kidney, all that was lost during nearly 1 wk of anoxia seemed to be regained in less than 40 min of normoxia. This might reflect an adaptive strategy. Because of the limited possibility of recovering catecholamines that have been released into the bloodstream, the crucian carp chromaffin tissue might have become very good at taking the opportunities given by short contacts with O2 to rapidly renew its catecholamine store.

Animals↗