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PubMed1989

Persistent effects of neonatal toluene exposure on regional brain catecholamine levels and turnover in the adult male rat.

Effects of neonatal toluene exposure (80 ppm, day 1-7, 6 h/day) have been studied on regional brain catecholamine levels and utilization, and on serum levels of hypophyseal and adrenocortical hormones in the adult male rat. Catecholamine levels were measured by quantitative histofluorimetry in the forebrain and hypothalamus and by high pressure liquid chromatography with electrochemical detection in the substantia nigra. Catecholamine utilization was evaluated from the decrease in catecholamines seen after tyrosine hydroxylase inhibition using alpha-methyl-p-tyrosine methyl ester hydrochloride (alpha MT, 250 mg/kg, i.p., 2 h). Serum levels of thyroid stimulating hormone, corticosterone, aldosterone, prolactin and luteinizing hormone were measured by radioimmunoassays. Neonatal toluene exposure produced a reduction of dopamine levels and utilization selectively in the olfactory tubercle and substantia nigra of the adult rat. Furthermore, neonatal toluene exposure produced a significant reduction in the noradrenaline levels and utilization in the substantia nigra and an increase of noradrenaline utilization selectively in the subependymal layer of the median eminence and of the magnocellular part of the paraventricular hypothalamic nucleus. The serum hormone levels were not significantly influenced by neonatal toluene exposure as evaluated in adulthood. However, the alpha MT induced increase in serum prolactin levels was reduced following neonatal exposure to toluene. Neonatal toluene treatment was also found to alter the responses of the catecholamine neurons to subacute toluene exposure in adulthood. In some of the dopamine nerve terminal systems of the forebrain and in the dopamine cell body containing area of the substantia nigra neonatal toluene exposure appears to have made the dopamine neurons insensitive to adult subacute toluene exposure. In the hypothalamic noradrenaline nerve terminal systems, there were even reversed responses to subacute toluene exposure. The present results indicate that neonatal toluene exposure in doses at the threshold limit value produces persistent changes in dopamine and noradrenaline neurons of the forebrain, hypothalamus and substantia nigra in the presence of a relatively intact neuroendocrine system. In addition, neonatal toluene exposure appears to diminish or even counteract the responses to subacute toluene treatment in adulthood.

Administration, Inhalation↗
PubMed1981

Effect of thyroid status on alpha- and beta-catecholamine responsiveness of hamster adipocytes.

It has been suggested that part of the increased beta-catecholamine responsiveness in hyperthyroid animals is due to a decrease in alpha-catecholamine action. The present results indicate that neither hyperthyroidism nor hypothyroidism altered the alpha 2-adrenergic inhibition of adenylate cyclase or the alpha 1-adrenergic stimulation of phosphatidylinositol turnover in adipocytes from the white adipose tissue of hamsters. No effect of hyperthyroidism was found on the Kd for binding of [3H]dihydroergocryptine or the number of binding sites in membranes prepared from hamster adipocyte tissue. The stimulation of cyclic AMP due to beta-catecholamines was enhanced in adipocytes from hyperthyroid hamsters, as was lipolysis. However, in adipocytes from hyperthyroid hamsters the maximal stimulation of cyclic AMP due to isoproterenol, ACTH or epinephrine plus yohimbine, as seen in the presence of adenosine deaminase and theophylline, was less than in adipocytes from euthyroid hamsters. The activation of adenylate cyclase by isoproterenol was the same in membranes from hyperthyroid as compared to those from euthyroid hamsters in the absence or presence of guanine nucleotides. These data suggest that thyroid status has little effect on alpha-catecholamine action by enhances the activation of lipolysis by beta-catecholamine agonists.

Adipose Tissue↗
PubMed1989

cis-unsaturated fatty acids stimulate catecholamine secretion, tyrosine hydroxylase and protein kinase C in adrenal medullary cells.

In digitonin-permeabilized bovine adrenal medullary cells, arachidonic acid and oleic acid, the cis-unsaturated fatty acids, enhanced Ca2+-induced secretion of catecholamines, whereas elaidic acid, a trans-unsaturated fatty acid and stearic acid, a saturated fatty acid, had no effect. Indomethacin, an inhibitor of cyclooxygenase and nordihydroguaiaretic acid, an inhibitor of lipoxygenase, failed to inhibit the stimulatory effect of arachidonic acid. Stimulation of catecholamine secretion by arachidonic acid was abolished by the removal of adenosine 5'-triphosphate and Mg2+ from the incubation medium. Pretreatment of the cells with phorbol 12-myristate 13-acetate, an activator of protein kinase C, enhanced Ca2+-induced catecholamine secretion. In cells pretreated with phorbol 12-myristate 13-acetate, the stimulatory effect of arachidonic acid on Ca2+-induced catecholamine secretion was greatly reduced. In digitonin-permeabilized cells, arachidonic acid and oleic acid enhanced Ca2+-induced activation of tyrosine hydroxylase in the presence of adenosine 5'-triphosphate and Mg2+, whereas elaidic acid and stearic acid did not activate the enzyme. In a soluble fraction of adrenal medullary cells, 32P incorporation to histone by protein kinase C was increased by arachidonic acid and oleic acid, but not by elaidic acid and stearic acid. These results suggest that cis-unsaturated fatty acids modulate Ca2+-induced catecholamine secretion and tyrosine hydroxylase activity by activation of protein kinase C in adrenal medullary cells.

Adenosine Triphosphate↗
PubMedDate not supplied

Catecholamine neurons in the brain stem of tree shrew (Tupaia).

Glyoxylic acid-paraformaldehyde-induced histofluorescence was used to determine locations of catecholamine-containing neurons in the brain stem of Tupaia. Fluorescent cells in the medulla were located ventrolaterally in association with the lateral reticular nucleus; another group was found dorsolateral to the hypoglossal nucleus and extended laterally toward the solitary nucleus. In the pons, fluorescent cells were found in locus coeruleus, subcoeruleus and in association with the superior olivary nucleus. At caudal midbrain levels, catecholamine neurons were seen within the reticular formation and in association with the dorsal raphe nucleus, while more rostrally fluorescent neurons were located in substantia nigra, ventral tegmental area, among root fibers of the oculomotor nerve and in periaqueductal gray. The locations of catecholamine-containing neurons in tree shrew conform to the general mammalian pattern. Additionally, tree shrew has catecholamine neurons in the rostral mesencephalic periaqueductal gray as described in rat, opossum, rabbit and some primate; catecholamine neurons are also associated with the dorsal raphe nucleus in Tupaia, a finding previously reported only in primates.

Animals↗
PubMedDate not supplied

Coexistence of bovine pancreatic polypeptide-like immunoreactivity and catecholamine in neurons of the ventral aminergic pathway of the rat brain.

The coexistence of bovine pancreatic polypeptide (BPP) within the cell bodies and axons of noradrenergic neurons of the rat brain was studied. Adjacent hindbrain sections stained by the indirect immunofluorescence technique for either BPP or dopamine-beta-hydroxylase (DBH) revealed A1 and A2 cell bodies containing both antigens. Following bilateral knife cuts of the ventral noradrenergic bundle (VB), the localization of BPP, DBH and catecholamine within the VB and terminal fields of the hypothalamus was determined. An axoplasmic buildup of BPP immunofluorescent material was observed caudal to the knifecut together in the same axonal fields as catecholamine and DBH-containing axons. In the hypothalamus there was a marked decrease in the number of catecholamine-containing nerve fibers. However, there was no obvious decrease in the number of BPP fibers. The influence of high intraventricular doses of 6-hydroxydopamine on BPP and DBH-containing nerves in the hypothalamus was studied. While there was a marked reduction in DBH immunoreactive fibers, BPP fibers appeared relatively unchanged. These results suggest that BPP coexists within some hindbrain catecholamine neurons and their axons. It is suggested that BPP and catecholamine coexist in terminal fields within the hypothalamus. Failure to reveal a decrease in the BPP-fibers in these fields suggests that sprouting of arcuate nucleus derived non-aminergic BPP-containing fibers has occurred.

Adrenergic Fibers↗
PubMedDate not supplied

Relationship of catecholamines and LHRH: light microscopic study.

A wealth of evidence suggests that catecholamines influence gonadotrophin secretion. To assess whether this interaction involved LHRH cells or their processes, the distribution of the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH) was examined with reference to the LHRH system in the adult male mouse brain. Alternate 30-50 micron sections cut on a vibrating microtome were stained immunocytochemically for TH and LHRH. These studies revealed the presence of catecholamine fibers in the areas of LHRH cells. Co-localization of TH and LHRH with a dual immunoperoxidase technique in single 20-25 micron sections showed a juxtaposition of catecholamine fibers on LHRH cells and their dendrites. All LHRH cells did not appear contacted. In addition, LHRH axons were in close apposition to the dopamine cells of the arcuate nucleus and periventricular hypothalamus. Within the median eminence, the anatomical distribution of LHRH and TH was differentially organized with few areas of overlap. These results support a direct action of catecholamines on the LHRH system and suggest that LHRH may influence dopamine function.

Animals↗
PubMed1984

Catecholamine innervation of cervical dendrite bundles: possible phrenic nucleus innervation.

The catecholaminergic innervation of three recently described dendrite bundles (midline, central and lateral) in the cervical spinal cord of the adult Long-Evans hooded rat [41] was examined using Golgi impregnation, fluorescence histochemistry for catecholamines, and cholinesterase histochemistry. The midline and lateral bundles were similar in appearance to those described by the Scheibel and Scheibel [50,51], while the central bundle, present in the region of the phrenic nucleus, has not been described previously. Analysis of Golgi-Cox impregnated horizontal sections demonstrated the presence of fine varicose fibers within all three bundles. These profiles entered the bundles at right angles, either singly or within small transverse dendritic subunits, then turned in a rostral or caudal direction, and coursed adjacent to dendrites of motoneurons in the bundles. Catecholamine histofluorescence in horizontal sections revealed abundant varicosities within all three bundles, similar in size and appearance to the varicose fibers seen in Golgi-Cox impregnated sections. Catecholamine fibers entered the dendrite bundles at right angles then turned rostrally or caudally and coursed horizontally within the bundles. Varicose fluorescent profiles formed pericellular rings around the motoneurons and linear profiles adjacent to the dendrites, sometimes outlining the entire proximal portion of primary dendrites. Catecholamine fibers entered the dendrite bundles at right angles then turned rostrally or caudally to course adjacent to the dendrites within the bundles. Cholinesterase histochemistry in alternate sections revealed staining of motoneurons and their dendrites, and confirmed the location of the catecholamine varicosities within the motoneuron dendrite bundles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

MPTP alters central catecholamine neurons in addition to the nigrostriatal system.

The present studies were undertaken to determine if MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) treatment in mice alters catecholamine or serotonin systems of the brain in addition to reported effects on the dopaminergic nigrostriatal system. Male Swiss-Webster mice were injected with 30 mg/kg MPTP daily for three days. Treated and control animals were sacrificed 10 and 24 days after the last injection, and brains were prepared for serotonin immunocytochemistry and catecholamine histofluorescence. MPTP treatment resulted in a reduced number of neurons and a reduced intensity of the fluorescence in the remaining cell bodies of substantia nigra pars compacta. A reduced presence of catecholamine varicosities in the medullary raphe nuclei and the ventromedial reticular formation of the medulla was observed. Immunocytochemical studies revealed no alteration in the number of serotonin positive cell bodies in the dorsal and median raphe nuclei. We suggest that MPTP treatment selectively alters some non-nigrostriatal catecholamine systems of the brain stem in addition to its toxic effects on the dopaminergic nigrostriatal system, while leaving other non-nigrostriatal catecholamine systems intact.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Effect of catecholamines and metal chelating agents on the brain and brown adipose tissue Na,K-ATPase.

Catecholamines stimulate Na,K-ATPase activity in the microsomal membranes of the brain and brown adipose tissue. This stimulation is apparent in the absence of soluble, cytosolic inhibitors and exhibits the same characteristics in both tissues: it occurs at high concentrations (10(-6)-10(-4) M) only; there is no difference in potency between isoprenaline, norepinephrine and epinephrine (EC50 = 1-2 X 10(-5) M); the D-stereoisomer of isoprenaline is equally as effective as the L-form; stimulation of Na,K-ATPase may also be achieved by the metal chelators EDTA, EGTA and desferal; the hydrophobic beta-blockers, propranolol and alprenolol, inhibit both the norepinephrine-stimulated and basal levels of enzyme activity at concentrations of 10(-5)-10(-3) M; phenoxybenzamine, an irreversible alpha-adrenergic blocker, inhibits basal Na,K-ATPase as well as norepinephrine-stimulated enzyme activity (EC50 = 2.5 X 10(-5) M). Because none of these observations can be related to the properties of the stereospecific adrenergic receptor (alpha or beta), it may be concluded that the catecholamine-Na,K-ATPase interaction is not mediated by the receptor. More probably, catecholamines may antagonize the Na,K-ATPase inhibition caused by some tightly membrane-bound metals (but not vanadium) via the ortho-catechol moiety of the catecholamine molecule. The stimulation of brown fat Na,K-ATPase by catecholamines does not have much relevance to the norepinephrine-stimulated thermogenesis in this tissue.

Adipose Tissue, Brown↗
PubMed1995

Do synthetic adrenergic agents interfere with the measurement of endogenous plasma catecholamine concentrations?

PURPOSE: It is common to administer synthetic sympathomimetic and sympatholytic agents in the intensive care unit and operating room. The present study examines whether such agents, as well as the products of catecholamine metabolism, interfere with the quantitation of endogenous catecholamines by high-performance liquid chromatography. METHODS: Samples of drugs and metabolites were assayed before and after alumina extraction and their relative retention times were compared with dopamine, norepinephrine, and epinephrine relative retention times. Blood samples from patients receiving these drugs were also assayed for their interferences with catecholamine determination. RESULTS: Phenylephrine interfered with the quantitation of epinephrine. Isoproterenol's peak was so delayed it appeared in the following chromatogram. Dobutamine had two small peaks in vitro, whereas in the patient samples only one peak was identified; the other was probably masked by the dopamine peak. Labetalol had one peak when the pure drug was assayed but multiple peaks in patient samples, that were probably caused by metabolites of labetalol. CONCLUSION: Synthetic adrenergic agents and catecholamine metabolites can potentially interfere with the quantitation of the endogenous catecholamines. Thus, it is important to examine whether such interference occurs when conducting high-performance liquid chromatography assays.

Adrenergic Agents↗
PubMed1995

The effects of L-dihydroxyphenylalanine on alertness and mood in alpha-methyl-para-tyrosine-treated healthy humans. Further evidence for the role of catecholamines in arousal and anxiety.

Treatment with alpha-methyl-para-tyrosine (AMPT), a catecholamine synthesis inhibitor, has been shown to produce pronounced increases in sleepiness and mild increases in negative mood and anxiety when administered to healthy male adults. The present study was conducted to ascertain whether these effects of AMPT are secondary to decreases in brain catecholamines or whether they represent nonspecific drug effects. Forty-one healthy males were randomized to one of four treatment groups. (1) Treatment with AMPT alone (AMPT/placebo); (2) treatment with AMPT plus L-dopa/carbidopa (AMPT plus L-dopa/carbidopa); (3) treatment with L-dopa/carbidopa alone (placebo plus L-dopa/carbidopa); or (4) treatment with placebo alone (placebo plus placebo). Repeated measures of alertness, mood, and anxiety were obtained over a three-day period of drug treatment and following drug discontinuation. As before, AMPT treatment led to increased sleepines. In addition, AMPT treatment led to decreased calmness, increased tension and anger, and a trend for increased depression. Replacement of catecholamine stores with L-dopa reversed the effects of AMPT and was associated with a more rapid recovery from AMPT's effects. These findings indicate that AMPT's effects on alertness and anxiety are catecholamine-specific. Further, they provide additional evidence that catecholamines are involved in the regulation of normal states of arousal, and they are consistent with the view that brain catecholaminergic dysregulation is involved in pathological anxiety states.

Adult↗
PubMed1993

Activation of adrenal medullary L-arginine: nitric oxide pathway by stimuli which induce the release of catecholamines.

The activation of the L-arginine: nitric oxide (NO) pathway in the cat adrenal medulla by different stimuli which induce the release of catecholamines was studied. Stimuli that evoke catecholamine release, such as electrical stimulation of splanchnic nerves (50 V, 5 Hz, 1 ms), methacholine (100 microM), dimethyl-4-phenylpiperazinium iodide (DMPP; 10 microM), high K+ (35 mM) and alamethicin (15 micrograms ml-1) also caused a rise in cyclic GMP in the perfused cat adrenal medulla. NG-nitro-L-arginine methyl ester (L-NAME; 1 mM) abolished the rise in cyclic GMP induced by these stimuli without affecting the catecholamine release. Bovine adrenal medulla cytosol contained an NO synthase which was L-arginine- and Ca(2+)-dependent. In conclusion cat and bovine adrenal medulla stimulated with a variety of secretagogues synthesize NO from L-arginine to activate the soluble guanylate cyclase. The present data do not rule out a role for cyclic GMP in the regulation of catecholamine secretion; however, it seems more plausible that cyclic GMP may play a role in controlling local blood flow and thus the access of the released catecholamines to the systemic circulation during stressful conflicts.

Adrenal Medulla↗
PubMed2005

Novel stressors affected catecholamine stores in socially isolated normotensive and spontaneously hypertensive rats.

Catecholamines in some central (hypothalamus and hippocampus) and peripheral tissues (adrenal glands and heart auricles) of long-term socially isolated normotensive and spontaneously hypertensive rats exposed to novel immobilization stress were determined by a simultaneous single isotope radioenzymatic assay. Long-term isolation (21 days) produced depletion of hypothalamic norepinephrine (NE) stores and hippocampal dopamine (DA) stores in both normotensive and spontaneously hypertensive rats. Acute immobilization stress (2 h) significantly decreased NE and DA stores in hypothalamus and hippocampus of naive normotensive and spontaneously hypertensive rats controls. However, novel immobilization stress applied to normotensive rats previously subjected to long-term isolation produced no changes in catecholamine levels in hypothalamus, while resulting in somewhat higher depletion of NE stores in hypothalamus of spontaneously hypertensive rats treated in the same way. Novel immobilization stress decreased NE and DA stores in hippocampus of normotensive but was without effect on NE and DA stores of spontaneously hypertensive rats. Social isolation did not affect catecholamine stores in peripheral tissues but novel immobilization stress produced a significant decrease in catecholamine content. The results suggest that some central and peripherals tissues of spontaneously hypertensive rats and normotensive rats differ with regard to catecholamine content and that there are certain differences in their responsiveness to stress.

Adrenal Glands↗
PubMed2006

Catecholamines and development of cardiac pacemaking: an intrinsically intimate relationship.

A generation ago, a melding of imagination and experimental evidence led to the hypothesis that catecholamines were essential in establishing basal cardiac pacemaking rhythm. Subsequent discoveries of depolarizing "pacemaker" currents and viable adult catecholamine-deficient animals raised serious doubts about the necessity of catecholamines in pacemaking. However, the findings that catecholamines are produced in pacemaking regions prior to innervation, and that they are required for embryonic survival during a defined "critical period" of embryonic development have revitalized the original hypothesis. Recent results have further suggested that intrinsic cardiac adrenergic cells can differentiate into pacemaking myocytes, and that protein kinase A, a prominent downstream mediator of beta-adrenergic signaling, is required for pacemaking activity. Here, we discuss how catecholamines and the intrinsic cardiac adrenergic cells that produce them may influence ontological development of cardiac pacemaking.

Animals↗
PubMed2004

Immunomodulatory function of seminal catecholamines may be an adaptation for reproduction.

Catecholamines are found at high concentrations in seminal fluid. The exact functional significance of seminal catecholamines is unknown. We hypothesize that seminal catecholamines perform important immunomodulatory functions that support reproductive success. Specifically, we propose that catecholamines contribute to a local adaptive shift of T helper (Th) balance to Th2 dominance in the maternal reproductive tract to enable the gametes, and possibly the nascent zygote, to evade immune surveillance of the female. Our hypothesis suggests that the Th2 effects of catecholamines are independent of the direct immunomodulatory effects of seminal cytokines such as prostaglandin E2 and transforming growth factor beta1. Potential immunomodulatory functions of other seminal constituents such as aldosterone, oxytocin, vasopressin, and angiotensin remain unexplored and represents a topic of future interest. Seminal stress hormones may play a role in mating dynamics since alpha males typically live in a state of high hormonal stress, Mating with adrenalized alpha males may represent an adaptive Darwinian strategy by females to maximize their reproductive fitness.

Adaptation, Physiological↗
PubMed2004

Effect of pramlintide on symptom, catecholamine, and glucagon responses to hypoglycemia in healthy subjects.

Pramlintide is an analog of the human glucoregulatory hormone amylin. Previous studies have shown no clear evidence that pramlintide modifies the response to insulin-induced hypoglycemia; however, a detailed assessment of responses at hypoglycemic thresholds has not been conducted. To further test the effect of pramlintide on symptom, catecholamine, and glucagon responses, a 3-step hypoglycemic clamp was investigated in healthy volunteers. In a randomized, double-blind, placebo-controlled, crossover study, 18 healthy subjects without diabetes received subcutaneous premeal injections of either placebo or 60 microg pramlintide 3 times daily for 5 consecutive days. On day 6, subjects received study drug with breakfast and, after a 7-hour fast, were connected to a Biostator for a 3-step, 3-hour clamp experiment (insulin infusion rate: 1.0 mU/kg/min; blood glucose targets: 70, 55, and 45 mg/dL). An intravenous (IV) infusion of pramlintide (16 microg/h) or placebo was initiated at t = 60 minutes. At the end of each 60-minute clamp step, autonomic (sweating, palpitations, hunger, etc) and neuroglycopenic (confusion, headache, odd behavior, etc) symptoms were assessed using a validated visual analog scale questionnaire. Blood samples were collected at 30-minute intervals for measurement of plasma glucose, insulin, pramlintide, catecholamine, and glucagon concentrations. Intraindividual and group mean responses showed that autonomic symptoms and plasma catecholamine and glucagon concentrations increased progressively during the clamp, with no discernible differences between pramlintide and placebo treatments. Group means for catecholamines at 60 minutes were: epinephrine 233 +/- 42, 892 +/- 85, 2,340 +/- 302 and 202 +/- 25, 774 +/- 114, 2,751 +/- 404 pg/mL and norepinephrine 1,138 +/- 86, 1,236 +/- 77, 1,721 +/- 158 and 1,278 +/- 108, 1,259 +/- 109, 1,580 +/-136 pg/mL (+/- SEM) for placebo- and pramlintide-treated groups at 70, 55, and 45 mg/dL glucose, respectively. Group means for glucagon were 72 +/- 6.3, 98 +/- 11.1, 130 +/- 14.7 and 63 +/- 3.6, 92 +/- 9.4, 120 +/- 16.0 pmol/L (+/- SEM) for placebo- and pramlintide-treated groups at 70, 55, and 45 mg/dL glucose, respectively. These results showed that pramlintide did not impair the symptom, catecholamine, and glucagon responses to insulin-induced hypoglycemia in healthy subjects.

Adolescent↗
PubMed2006

Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals.

OBJECTIVE: This study examined the hypothesis that intracellular cGMP stimulates the release of catecholamines from sympathetic nerve terminals (SNTs) in conscious rats. METHODS: Conscious rats were prepared to determine the effects of intravenously-administered agents on heart rate (HR) and mean arterial blood pressure (MAP). RESULTS: Bolus intravenous injections of the membrane-permeable cGMP analogue, 8-(4-chlorophenylthio)-cGMP (8-CPT-cGMP), elicited immediate and pronounced increases in HR before any changes in MAP were observed. In contrast, injections of cGMP did not elicit changes in HR or MAP. The 8-CPT-cGMP-induced tachycardia was markedly diminished by (1) the beta(1,2)-adrenoceptor antagonist, propranolol, (2) the ganglion blocking agent, chlorisondamine, and (3) bretylium, which blocks Ca2+-dependent mobilization of vesicular stores of catecholamines from SNTs. 8-CPT-cGMP also elicited minor falls in MAP in propranolol-treated rats but elicited pronounced falls in MAP in rats treated with chlorisondamine, bretylium, or combined administration of bretylium and the muscarinic receptor antagonist, methyl-atropine. CONCLUSIONS: These findings suggest that (1) intracellular cGMP elicits the release of Ca2+-sensitive and Ca2+-insensitive stores of catecholamines from SNTs in conscious rats, and (2) cGMP-mediated release of catecholamines from SNTs antagonizes cGMP-mediated relaxation of vascular smooth muscle in resistance arteries. Taken together, these findings support the concept that increases in intracellular cGMP levels by atrial natriuretic peptide and endothelium- and cardiac-derived nitric oxide regulate sympathetic control of the heart and the microvasculature of conscious rats via cGMP-dependent release of catecholamines.

Animals↗
PubMed2004

Dual mode of catecholamine action on splenic macrophage phagocytosis in wall lizard, Hemidactylus flaviviridis.

In the present study, in vitro concentration-related effect of catecholamines, dopamine (DA), norepinephrine (NE), and epinephrine (E) was observed on phagocytic activity of splenic macrophages to understand the impact of sympatho-adrenal-medullary (SAM) activation on innate immunity in wall lizard Hemidactylus flaviviridis under stress condition. Restraint stress for 1 h resulted in marked suppression of macrophage phagocytosis, suggesting that supra-physiological level of catecholamines in response to SAM activation under stress suppressed phagocytosis. This interpretation was reinforced since all the catecholamines considerably reduced phagocytosis at high concentrations ranging from 10(-7) to 10(-5)M. On the contrary, DA, NE, and E at low concentrations considerably stimulated phagocytosis, which increased with the decrease of concentrations ranging from 10(-11) to 10(-15)M. Further, effect of NE and E was blocked by beta-adrenergic blocker suggesting the beta-adrenoceptor-dependent regulating mechanism of NE and E. DA acts through both beta-adrenoceptor-dependent and D1/D2 class receptor-dependent mechanism, since beta-adrenergic blocker could partially block the DA effect. beta-Adrenoceptor-linked adenylate cyclase-mediated cAMP action in modulation of phagocytic activity was evident as 3-isobutyl-1-methyl-xanthine suppressed phagocytosis. Further, to delineate the mode of dual effect of catecholamines through beta-adrenergic receptors, in vitro concentration-related effect of cAMP was investigated on macrophage phagocytosis. cAMP depending on concentration had opposite effect on phagocytosis, and its stimulatory effect at low concentrations was reversed by actinomycin D and cycloheximide, whereas these transcription and translation inhibitors, respectively, failed to alter the inhibitory effect of cAMP at high concentrations. This suggests the concentration-related two different pathways of catecholamine action, classical non-genomic at high concentration while genomic pathway at low concentration.

1-Methyl-3-isobutylxanthine↗