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PubMed1987

Early increase in adrenomedullary catecholamine synthesis in sinoaortic denervated rats.

Adrenomedullary catecholamines (dopamine, noradrenaline and adrenaline) and catecholamine synthesizing enzymes (tyrosine hydroxylase and dopamine beta-hydroxylase) were elevated within 3 days of sinoaortic denervation in rats with neurogenic hypertension. Conversely, there were no differences in adrenomedullary catecholamines and their related enzymes 21 days after sinoaortic denervation. These results suggest an activation of adrenomedullary catecholamine synthesis at the onset of neurogenic hypertension.

Adrenal Medulla↗
PubMed1988

5-Hydroxytryptamine and catecholamines in developing sympathetic cells of the rat.

Appearance of 5-hydroxytryptamine (5-HT) in developing sympathetic cells of prenatal rats was studied using the indirect immunofluorescence method. In consecutive sections, tyrosine hydroxylase (TH) immunoreactivity was considered as a marker for catecholamine-synthesizing cells in general, while phenylethanolamine N-methyltransferase (PNMT) immunoreactivity was used as an indicator of adrenaline synthesis. 5-HT immunoreactivity was observed for the first time in 12.5-day-old embryos in developing sympathetic chain ganglia. On day 13.5, 5-HT-immunoreactive cells were first seen on the preaortic region and on day 14.5 in the developing adrenal gland. Comparison with consecutive sections stained for TH revealed that all TH-immunoreactive cells were also 5-HT-immunoreactive. During later development, however, 5-HT immunoreactivity was retained by some cell types in each sympathetic tissue. In the ganglia, most developing principal nerve cells gradually lost their 5-HT immunoreactivity, while all so-called small intensely fluorescent (SIF) cells remained intensely 5-HT-immunoreactive. In the adrenal medulla, all catecholamine-containing cells showed 5-HT immunoreactivity until day 16.5. The first adrenaline-synthesizing cells appeared at this stage. Occasionally on day 16.5 and constantly on day 17.5 noradrenaline cell islets were distinguished among adrenaline cells. The adrenaline cells retained intense 5-HT immunoreactivity, while the noradrenaline cells were non-reactive to it. In the main retroperitoneal paraganglion, two noradrenaline cell populations were distinguished from day 15.5, one being 5-HT-immunoreactive and the other non-reactive. A third population appeared in this tissue at the time of birth, consisting of adrenaline-synthesizing cells which were also 5-HT-immunoreactive. These results indicate that the 3 sympathetic tissues undergo similar developmental changes: 5-HT immunoreactivity occurs in conjunction with the initiation of catecholamine synthesis and appears first in all catecholamine cells. During maturation it is confined to certain subpopulations in each tissue, i.e. the SIF cells and some principal nerve cells of the ganglion, the adrenaline cells of the adrenal medulla, the adrenaline cells and some noradrenaline cells of the paraganglionic tissue.

Animals↗
PubMed1988

Postnatal development of catecholamines and response to hypoxia in adrenals and paraganglia of rabbits.

The postnatal development of catecholamine levels in adrenals and paraganglia in newborn rabbits has been analyzed. At birth, the dominant catecholamine was noradrenaline, contributing 66% of the total catecholamine pool at day 1, 55% of which came from the paraganglia. There was a rapid postnatal increase of adrenaline, which constituted 67% of the total catecholamines at day 6 and 97% in the adult. After hypoxia at day 1, the noradrenaline levels decreased in paraganglia but not in adrenals, while adrenaline levels did not significantly change in either organ.

Adrenal Glands↗
PubMed1995

Effects of hypercortisolemia or hyperinsulinemia on neurochemical indices of catecholamine release and synthesis in conscious rats.

Glucocorticoids and insulin (INS) complexly affect sympathoneural and adrenomedullary outflows. This study assessed effects of chronic hypercortisolemia and effects of INS independent of INS-induced hypoglycemia on neurochemical indices of different aspects of catecholaminergic function in conscious rats. Since L-DOPA is the precursor of the endogenous catecholamines and the immediate product of the rate-limiting enzymatic step in catecholamine biosynthesis, alterations in rates of appearance (spillover) of L-DOPA in arterial plasma may reflect alterations in catecholamine synthesis. The study therefore included examination of whether cortisol (CORT) or INS affects L-DOPA spillover or renal excretion of dopamine (DA) derived from plasma L-DOPA. Arterial plasma levels and urinary excretion rates of endogenous catechols and radiolabelled L-DOPA and DA were measured during systemic intravenous infusions of [3H]L-DOPA. CORT was administered via a subcutaneous minipump reservoir for one week prior to [3H]L-DOPA infusion, and INS was infused with glucose to examine effects of hyperinsulinemia independently of hypoglycemia. CORT decreased plasma levels and urinary excretion of norepinephrine (NE). INS did not. Neither CORT nor INS affected levels of other catechols, L-DOPA spillover, or the rate of urinary excretion of [3H]DA for a given plasma level of [3H]L-DOPA. The results suggest that CORT inhibits sympathetically-mediated NE release without altering overall rates of catecholamine turnover or synthesis in sympathetic nerves in vivo and that INS effects on catecholaminergic function depend entirely on INS-induced hypoglycemia.

Animals↗
PubMed1996

Hypotensive and hypertensive effects of catecholamines intrathecally injected in anesthetized rats.

The cardiovascular effects of catecholamines intrathecally (i.t.) injected at the T12-L1 level were analyzed in pentobarbital anesthetized rats. Volumes of injection were not greater than 3 microliters. Noradrenaline in doses ranging from 0.03 to 0.3 micrograms (i.t.) did not alter the mean blood pressure (MBP) while higher doses (1, 3 and 10 micrograms, i.t.) caused a dose-dependent increase in MBP. Adrenaline induced hypotensive effects at low doses (0.03-0.3 micrograms i.t.) and pressor effects at high doses (3 and 10 micrograms, i.t.). Neither adrenaline nor noradrenaline modified the heart rate. The pressor responses to both catecholamines were antagonized by the alpha 1-adrenoceptor blocker prazosin (0.05-1 microgram, i.t.) and by the selective alpha 1A-adrenoceptor antagonist 5-methyl urapidil (10 and 15 micrograms, i.t.). In contrast, these pressor effects were not modified by the alpha 1B-adrenoceptor antagonist chloroethylclonidine (90 micrograms i.t.). In animals pretreated with 1 microgram prazosin (i.t.), low doses of noradrenaline (0.03 and 0.1 microgram, i.t.) caused a hypotensive effect. Prazosin (1 microgram i.t.) failed to alter the hypotension caused by 0.1 microgram adrenaline. The hypotensive response induced by either 0.1 microgram noradrenaline (in the presence of prazosin) or 0.1 microgram adrenaline was blocked by the alpha 2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.), by the GABA-A antagonists bicuculline (3.2 micrograms, i.t.) and picrotoxin (2.7 micrograms, i.t.), and by the GABA-B antagonist 2-hydroxy saclofen (30 micrograms, i.t.). The glycine-receptor antagonist strychnine (25 micrograms, i.t.) did not modify the hypotension induced by either noradrenaline (in the presence of prazosin) or adrenaline. These findings suggest that in the low thoracolumbar spinal cord of pentobarbital-anesthetized rats, noradrenaline and adrenaline have excitatory as well as inhibitory effects on the control of the BP. The pressor responses of high doses of i.t. injected catecholamines could be mediated by the activation of spinal alpha 1A-adrenoceptors, although the participation of alpha 1B-adrenoceptors cannot be rule out entirely. The hypotensive responses induced by low doses of i.t. injected catecholamines seem to involve the activation of spinal alpha 2A-adrenoceptors and the stimulation of an inhibitory GABAergic neuron in the spinal cord.

Adrenergic Agonists↗
PubMed1986

Non-neurogenic adrenal catecholamine release in the neonatal rat: exocytosis or diffusion?

When subjected to stress, neonatal rats secrete adrenal catecholamines by a mechanism which does not require nerve stimulation. To test whether the non-neurogenic secretory mechanism involves exocytosis, we examined the effects of hypoxia (a non-neurogenic stimulus) and nicotine (a stimulus which simulates neurogenic input) on catecholamine levels and on the uptake of [3H]epinephrine into chromaffin granules. Hypoxia- and nicotine-induced depletion of catecholamines were both accompanied by a reduction in uptake, indicating a loss of granule integrity which is characteristic of exocytosis. Although a significant proportion of adrenal catecholamines was found to be extragranular, only the granular pool was involved in the secretory response.

Adrenal Medulla↗
PubMed1993

Sexually dimorphic effects of prenatal cocaine on adult sexual behavior and brain catecholamines in rats.

Exposure to cocaine in utero (10 mg/kg twice a day on days 11-18 of gestation) differentially altered adult sexual behavior, brain catecholamine levels and perhaps open field activity in male and female rats. Female rats exposed to cocaine were significantly inhibited in their sexual behavior when compared to saline-exposed controls. In contrast, males exposed prenatally to cocaine exhibited normal or even facilitated sexual behavior. In particular, the significantly shorter post-ejaculatory intromission intervals displayed by cocaine-exposed males indicated that these animals might have enhanced sexual arousal or motivation. In tests for open field activity, males consistently showed higher levels of rearing behavior than females. Prenatal cocaine tended to reduce rearing in females, but this effect was not significant. Cocaine-exposed male rats had significantly higher norepinephrine and dopamine levels in the preoptic area than saline-exposed controls, whereas cocaine did not affect catecholamine content in male hypothalamus, striatum, cortex or cerebellum. Cocaine- and saline-exposed females had similar catecholamine levels in all brain regions. These results suggest that exposure of developing animals to modest doses of cocaine during mid to late gestation results in long-lasting, sexually dimorphic alterations of adult sexual behavior and brain catecholamines in rats.

Animals↗
PubMed1996

The non-neurogenic catecholamine response of the fetal adrenal to hypoxia is dependent on activation of voltage sensitive Ca2+ channels.

We have investigated the cellular mechanisms underlying the catecholamine response of the fetal sheep adrenal to hypoxia before and after the development of adrenal innervation. Adrenals were collected before (80-100 days gestation: n = 7) and after (135-146 days gestation: n = 10) development of innervation and retrogradely perfused with oxygenated Krebs bicarbonate buffer in vitro via the renal vein. Adrenal hypoxia was induced by perfusion with hypoxic Krebs buffer (pO2 = 46.7 +/- 2.4 mm Hg) for 30 min periods in the presence and absence of hexamethonium (500 microM), Ca2+ (2.5 mM), nifedipine (1 microM) and KCl (10 mM). Hypoxia stimulated an increase (P < 0.001) in the output of noradrenaline at 80-100 days (3 min pre hypoxia, 0.18 +/- 0.07 nmol/3 min; 20 min hypoxia, 0.74 +/- 0.22 nmol/3 min) and at 135-146 days (3 min pre hypoxia, 0.53 +/- 0.20 nmol/3 min; 20 min hypoxia, 1.71 +/- 0.85 nmol/3 min). Adrenaline output was also higher (P < 0.001) than basal values (80-100 days, 0.11 +/- 0.06 nmol/3 min; 135-146 days, 0.53 +/- 0.15 nmol/3 min) after 20 min hypoxia (0.41 +/- 0.20 nmol/3 min and 1.35 +/- 0.56 nmol/3 min respectively). The catecholamine responses to hypoxia were abolished by removal of Ca2+ from the adrenal perfusate. There was a reduction (P < 0.05) in the catecholamine secretory response to hypoxia in the presence of nifedipine. Noradrenaline output decreased from 4.33 +/- 0.84 nmol/30 min to 0.16 +/- 0.49 nmol/30 min and adrenaline output decreased from 3.16 +/- 1.66 nmol/30 min to -0.01 +/- 0.24 nmol/30 min in the presence of nifedipine. The fetal adrenal secretes catecholamines by a direct or non-neurogenic mechanism in response to hypoxia. This secretory response is dependent on the activation of voltage sensitive Ca2+ channels in the chromaffin cell membrane.

Adrenal Cortex↗
PubMed1986

Interactions of insulin, catecholamines and adenosine in the regulation of glucose transport in isolated rat cardiac myocytes.

The regulation of the glucose transport system by catecholamines and insulin has been studied in isolated rat cardiomyocytes. In the basal state, 1-isoproterenol exhibited a biphasic concentration-dependent regulation of 3-O-methylglucose transport. At low concentrations (less than 10 nM), isoproterenol induced a maximal inhibition of 65-70% of the basal rates, while at higher concentrations (greater than 10 nM) a 25-70% stimulation of transport was observed. In the presence of adenosine deaminase, the inhibition of isoproterenol at low doses was attenuated. No effect of adenosine deaminase was observed on the stimulation of transport at high doses of isoproterenol. The inhibitory effect of isoproterenol returned when N6-phenylisopropyladenosine (a non-metabolizable analog of adenosine) was included along with adenosine deaminase. Dibutyryl cAMP and forskolin both inhibited basal transport rates. In the presence of maximally stimulating concentrations of insulin, cardiomyocyte 3-O-methylglucose transport was generally elevated 200-300% above basal levels. In the presence of isoproterenol, insulin stimulation was inhibited at both high and low concentrations of catecholamine, with maximum inhibition occurring at the lowest concentrations tested. When cells were incubated with both adenosine deaminase and isoproterenol, the inhibition of the insulin response was greater at all concentrations of catecholamine and was almost completely blocked at isoproterenol concentrations of 10 nM or less. Dibutyryl cAMP inhibited the insulin response to within 10% of basal transport levels, while forskolin completely inhibited all transport activity in the presence of insulin. These results suggest that catecholamines regulate basal and insulin-stimulated glucose transport via both cAMP-dependent and cAMP-independent mechanisms and that this regulation is modulated in the presence of extracellular adenosine.

3-O-Methylglucose↗
PubMed1991

Osmotic strength differentiates between two types of calcium transport pathways regulating catecholamine secretion from cultured bovine chromaffin cells.

Calcium transport and catecholamine secretion was measured in cultured bovine chromaffin cells. Calcium ions which entered the cells following stimulation with either nicotine or 50 mM KCl (high potassium) triggered catecholamine release, but then inactivated the secretory process. The nicotine and the high potassium-induced calcium transport mechanisms were mechanistically distinct, but functionally dependent on each other. The specific evidence is that whereas the high potassium-induced Ca2+ influx was found to be inhibited by hyperosmotic medium, the nicotine-stimulated calcium influx was unaffected under these conditions. High potassium and nicotine-stimulated catecholamine release were also differently affected by hyperosmotic medium. While potassium-stimulated catecholamine release was profoundly inhibited by hyperosmolarity, nicotine-stimulated release was only moderately inhibited. Sequential treatments of cells with nicotine and high potassium, under isotonic physiological conditions, indicate that there is a functional, biochemical communication between the otherwise mechanistically distinct calcium channels. Calcium ions which were found to inactivate these channels may be the basis for such communication.

Adrenal Medulla↗
PubMed1991

Genes for human catecholamine-synthesizing enzymes.

Catecholamine neurotransmitters--dopamine, noradrenaline (norepinephrine), adrenaline (epinephrine)--are synthesized in catecholaminergic neurons from tyrosine, via dopa, dopamine and noradrenaline, to adrenaline. Four enzymes are involved in the biosynthesis of adrenaline: (1) tyrosine 3-mono-oxygenase (tyrosine hydroxylase, TH); (2) aromatic L-amino acid decarboxylase (AADC, or DOPA decarboxylase, DDC); (3) dopamine beta-mono-oxygenase (dopamine beta-hydroxylase, DBH); and (4) noradrenaline N-methyltransferase (phenylethanolamine N-methyltransferase, PNMT). We cloned full-length complementary DNAs (cDNAs) and genomic DNAs of human catecholamine-synthesizing enzymes (TH, AADC, DBH, PNMT) and determined the nucleotide sequences and the deduced amino acid sequences. We discovered multiple messenger RNAs (mRNAs) of human TH, human DBH, and human PNMT. Four types (types 1, 2, 3, and 4) of human TH mRNAs are produced by alternative mRNA splicing mechanism from a single gene. We found the multiple forms of TH in two species of monkeys, but only a single mRNA corresponding to human TH type 1 in Sunkus murinus and rat, suggesting that the multiplicity of TH mRNA is primate-specific. Total TH mRNA, especially the most abundant type 2 and type 1 mRNAs in the human brain, were found to be reduced during the process of aging. The multiple forms of human TH may give additional regulation to the human enzyme, probably through altered phosphorylation and activation. We have succeeded in producing transgenic mice carrying multiple copies of the human TH gene in brain and adrenal medulla. The level of human TH mRNA in brain was about 50-fold higher than that of endogenous mouse TH mRNA. In situ hybridization demonstrated an enormous region-specific expression of the transgene in substantia nigra and ventral tegmental area. TH immunoreactivity in these regions, Western blot analysis, and TH activity measurements proved definitely increased TH in transgenic mice, though not comparable to the increment of the mRNA. However, catecholamine levels in transgenics were not significantly different from those in non-transgenics. The results suggest complex regulatory mechanisms for human TH gene expression and for the catecholamine levels in transgenic mice. Kohsaka and Uchida in collaboration with us applied genetically engineered (human TH cDNA-transfected) non-neuronal cells to brain tissue transplantation in parkinsonian rat models. We isolated and sequenced a full-length cDNA encoding human AADC.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1993

Neuroimmune modulation: signal transduction and catecholamines.

In recent years, much interest has centered on the commonalities and bi-directional interactions between the nervous system and the immune system. This review focuses on mechanisms through which, catecholamines, a class of neuro-endocrine molecules, modulate immune functions. Catecholamines can be immune suppressive and inhibit lymphocyte activation of both T and B cells as well as the generation of immune-mediated anti-tumor responses. Some of these catecholamine-regulated activities appear to be modulated through the second messenger, cyclic AMP, whereas others appear to be catecholamine-dependent but cyclic AMP independent. Further delineation of the interacting ligand-receptor complexes, populations of responding cells and signal transduction mechanisms leading to the activation of specifically involved genes and gene products, will lead to enhanced understanding of the integratory functions of the nervous system in immune responses, the biology of stress, the role of stress-associated molecular mechanisms in perturbations of physiological homeostasis and the development of a new biological psychiatry with accompanying rational therapeutic modalities.

Animals↗
PubMed1994

Cardiovascular responses and central catecholamines in streptozocin-diabetic rats.

Brain catecholamine levels, spinal cord levels of the norepinephrine metabolite methoxy-hydroxy-phenylglycol (MHPG), and heart rate were measured in nondiabetic and streptozocin-diabetic rats after sham surgery or bilateral carotid ligation. Although carotid ligation increased heart rate in both diabetic and nondiabetic rats, in diabetic animals the response did not differ from the response to sham surgery. Carotid ligation increased epinephrine concentrations in the medulla/pons of diabetic animals but was not associated with alterations in other central catecholamines. In all diabetic rats spinal ratios of MHPG/norepinephrine (an index of noradrenergic activity) were higher than in nondiabetics, and the change in heart rate (post-surgical-pre-surgical rate) correlated inversely with hypothalamic dopamine (R = -0.60). In sham-operated diabetic rats there were high inverse correlations of the change in heart rate with medullary epinephrine and of pre- and post-surgical heart rate with spinal MHPG/NE (R = -0.87 to -0.95). Central catecholamines and heart rate were not correlated in nondiabetic animals and correlated only weakly when nondiabetic and diabetic animals were pooled. Correlations in diabetic animals were usually abolished or reduced by carotid ligation. These findings suggest a link between central catecholamines and heart rate in diabetic rats subjected to surgical stress. Whether catecholaminergic neurons contribute to abnormal chronotropic responses in diabetic rats or respond to stimuli that affect both heart rate and neural function remains to be determined.

Animals↗
PubMed1985

Plasma and myocardial catecholamine levels in young and aged rats during halothane anesthesia.

Plasma and heart tissue catecholamines were measured in young (4-month) and aged (28-month) Sprague Dawley rats under unanesthetized conditions and following the induction of halothane anesthesia. Arterial blood pressure, blood gases, plasma and heart tissue norepinephrine, epinephrine and dopamine concentrations were measured in separate groups of unanesthetized and halothane anesthetized rats. Young and aged rats were tested under equal anesthetic levels and blood halothane concentrations were measured using gas chromatography. Aged rats required significantly less halothane to maintain anesthesia compared to young animals (7.25 +/- 1.43 vs. 14.91 +/- 0.93 mg/dL, p less than 0.05). Cardiovascular parameters were similar in young vs. aged rats under unanesthetized conditions, but blood pressure decreased significantly more in aged than in young rats during halothane anesthesia (43% vs. 17%, p less than 0.05). Heart tissue catecholamines were not different between young and aged and did not change during halothane anesthesia. Plasma norepinephrine concentrations were consistently elevated in aged vs. young rats under both unanesthetized and anesthetized test conditions, but there was no significant change in these levels from the unanesthetized to the anesthetized state. Results suggest that increased catecholamine levels in aged animals may be necessary to maintain a normal cardiovascular state under unanesthetized conditions and that catecholamines do not increase during the hypotensive state produced by halothane anesthesia in spite of marked hypotension.

Aging↗
PubMed1992

Blood lactate and catecholamine levels in the carbon monoxide-exposed rat: the response to elevated glucose.

Previous studies have shown that elevated blood glucose is detrimental to the outcome in acute carbon monoxide (CO) poisoning. The present goals were to characterize the blood lactate and catecholamine changes and to determine whether elevated blood glucose results in increases in the levels of these substances. Two groups of adult Sprague-Dawley, Levine-prepared, female rats (n = 22 each) were exposed to 2400 ppm CO for 90 min: one group received nothing (CO alone), while the other group was infused with a 50% glucose solution (4 ml/kg) (CO + glucose). The usual hypothermia, hypotension, bradycardia and hemoconcentration associated with acute severe CO poisoning were observed. Survival rates were 68% and 54% in the CO alone and CO + glucose groups, respectively. Arterial blood pressure tended to decline more in rats that died; the difference was significant in the CO + glucose group. In the CO alone group, plasma glucose concentration was significantly lower after CO exposure in rats that died than in survivors (35 +/- 15 vs. 99 +/- 16 mg/dl). In the CO + glucose group, glucose concentration was significantly higher after 45 min in rats that died (d) than in survivors (s) (447 +/- 29 vs. 324 +/- 31 mg/dl). Elevated blood glucose in the CO + glucose group failed to significantly increase blood lactate; however, lactate tended to be higher in rats that died in both groups [CO alone group: 175 +/- 17 (d) vs. 138 +/- 9 (s); CO + glucose group: 154 +/- 10 (d) vs. 143 +/- 8 (s)]. Plasma epinephrine and norepinephrine increased significantly 6-10-fold and 2-6-fold in each of the two groups, respectively; however, catecholamine levels were not related to either the administration of glucose or survival. With regard to CO poisoning in this animal model, the results do not support the hypotheses that elevated blood glucose exacerbates the increase in blood lactate, that increased catecholamine increases glucose, or that greater CO-induced hypoglycemia results from increased lactate production. The results do show that death is related to abnormally high or low blood glucose, but that it is not due to higher blood lactate or catecholamine levels.

Animals↗
PubMed1992

Catecholamines during cardiopulmonary resuscitation for cardiac arrest.

Serum catecholamines were measured during continued prolonged cardiopulmonary resuscitation and after 10 mg increments of intravenous epinephrine. This was part of an ongoing trial of 10 mg epinephrine versus placebo. Eight patients were in the placebo arm and seven in the epinephrine arm and the rhythms were two ventricular fibrillation, nine asystole and four electromechanical dissociation. Data were analysed by time from onset of the cardiac arrest and samples were analysed for levels of DHPG (dihydroxyphenylglycol) nor-epinephrine, epinephrine, DOPA (dihydroxyphenylalanine) and DOPAC (dihydroxyphenyl acetic acid). There was a significant (P < 0.001) difference between arterial and venous samples of epinephrine but not the other catecholamines. High levels of catecholamines were maintained in all time phases except for nor-epinephrine where significant (P < 0.0003) reduction occurred progressively after 20 min. Non-steady state kinetics were suggested between epinephrine and nor-epinephrine and DHPG and nor-epinephrine for the first 20 min. Very large increases in epinephrine were achieved with administered 10 mg epinephrine and this resulted in high DHPG levels supporting the experimental belief that exogenously administered epinephrine induces myocardial release of nor-epinephrine. This data supports the known effects of CPR on catecholamine release. It provides data on the other neurotransmitter hormones and supports the relationships shown in other animal and human data. It is suggested that supplementation with epinephrine during CPR may be unnecessary and the levels reached may be deleterious. Nor-adrenaline supplementation may be necessary after prolonged CPR.

Cardiopulmonary Resuscitation↗
PubMed1980

Glucocorticoid and catecholamine stimulation of amino acid transport in rat hepatocytes. Synthesis of a high-affinity component.

The kinetic properties of glucocorticoid and catecholamine stimulation of amino acid transport in freshly isolated rat hepatocytes were investigated. In the basal state (i.e., with hepatocytes incubated for 2 h in the absence of glucocorticoid or catecholamine), the saturable transport of alpha-aminoisobutyric acid (AIB) was accounted for mainly by a low-affinity component (Km for AIB approximately 5 mM). Hepatocyte exposure to cortisol (or dexamethasone), or to epinephrine for isoproterenol), for 2 h resulted in a 3- to 4-fold increase in the Vmax of a high-affinity component (Km for AIB approximately 1 mM) which was only weakly expressed in the basal state. Neither glucocorticoids nor catecholamines exerted a detectable effect on the low-affinity transport component. Cycloheximide prevented the emergence of the high-affinity component in hepatocytes exposed to dexamethasone or epinephrine. The results suggest that the stmulatory effect of glucocorticoids and catecholamines on amino acid transport in hepatocytes results from the synthesis of a high-affinity transport component.

Aminoisobutyric Acids↗
PubMed1988

Adenylate cyclase of catfish hepatocyte membranes: basal properties and sensitivity to catecholamines and glucagon.

Some characteristics of adenylate cyclase of catfish (Ictalurus melas) liver membranes were studied, and the effects of catecholamines and of glucagon were tested. The enzyme has an optimum temperature of 40 degrees C, and a Km for ATP of 0.16 mM at 30 degrees C, and requires Mg2+ for its activity. The enzyme activity is inhibited with a Ca2+ concentration higher than 5 X 10(-5) M, and enhanced with F- higher than 10(-4) M. The response of adenylate cyclase to GTP is biphasic, with a maximum of activity at 10(-5) M GTP. Catecholamines (epinephrine, norepinephrine, isoproterenol, phenylephrine) enhance cyclase activity. Propranolol inhibits the increase in enzyme activity induced by catecholamines, whereas phentolamine is ineffective. This indicates that catecholamines (phenylephrine included) activate adenylate cyclase through a beta-adrenergic mechanism. Glucagon (mammalian) has a smaller effect than epinephrine in increasing the enzyme activity of catfish hepatocyte membranes. This fact is the opposite of that observed for the cyclase activity of rat liver membranes.

Adenosine Triphosphate↗