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PubMed1995

On-column reduction of catecholamine quinones in stainless steel columns during liquid chromatography.

The chromatographic behavior of quinones derived from the oxidation of dopamine and N-acetyldopamine has been studied using liquid chromatography (LC) with both a diode array detector and an electrochemical detector that has parallel dual working electrodes. When stainless steel columns are used, an anodic peak for the oxidation of the catecholamine is observed at the same retention time as a cathodic peak for the reduction of the catecholamine quinone. In addition, the anodic peak exhibits a tail that extends to a second anodic peak for the catecholamine. The latter peak occurs at the normal retention time of the catecholamine. The origin of this phenomenon has been studied and metallic iron in the stainless steel components of the LC system has been found to reduce the quinones to their corresponding catecholamines. The simultaneous appearance of a cathodic peak for the reduction of catecholamine quinone and an anodic peak for the oxidation of the corresponding catecholamine occurs when metallic iron in the exit frit reduces some of the quinones as the latter exits the column. This phenomenon is designated as the "concurrent anodic-cathodic response." It is also observed for quinones of of 3,4-dihydroxybenzoic acid and probably occurs with o- or p-quinones of other dihydroxyphenyl compounds. The use of nonferrous components in LC systems is recommended to eliminate possible on-column reduction of quinones.

Animals↗
PubMed1998

Electrostimulation of catecholamine release in the eel: modulation by antagonists and autocrine agonists.

The innervated chromaffin cells of the eel (Anguilla rostrata) release norepinephrine (NE) and epinephrine (E), while a component of the macrovascular wall releases dopamine (DA). The release of the three catecholamines is governed by complex controls which include adrenergic, nicotinergic, muscarinergic, and opioid mechanisms. To gain insight into the interactions between neural and autocrine factors in stimulated catecholamine release, we investigated the effect of adrenergic (phentolamine and propranolol) and muscarinergic (atropine) receptor antagonists, and of autocrine opioids (met-enkephalin, codeine, and morphine) on electrostimulated catecholamine secretion in situ. The hind brain (close to the root of nerve IX) of anesthetized eels was stimulated at four different time points, and segments of the posterior cardinal vein or the caudal vein were perfused with a saline solution, with or without test substances. Electrostimulation (30 s) four times within a total study duration of 14 min increased the release of DA, NE, and E into the perfusate of the cardinal vein. The vessel contains the innervated adrenomedullary equivalent. In the noninnervated caudal vein electrical stimulation had no impact on total DA release, while there was a slight decrease of NE release and a slight increase of E release. In the cardinal vein, both the alpha-adrenergic receptor antagonist phentolamine and the beta-adrenergic receptor antagonist propranolol strongly reduced the effect of electrostimulation on catecholamine release. Met-enkephalin reduced the release of all three catecholamines to a similar degree; its impact on NE release was especially strong. Codeine reduced the catecholamine release moderately, while morphine had no effect. Atropine reduced the release of all three catecholamines in a pattern similar to that of met-enkephalin. The findings on the posterior cardinal vein indicate that neurally stimulated NE and E release (1) involves autocrine/paracrine adrenergic mechanisms, (2) involves a muscarinergic mechanism, and possibly also endogenous codeine and morphine; and (3) is antagonized by met-enkephalin. The findings on the caudal vein are further evidence that macrovascular DA release is not under direct neural control.

Adrenergic Agonists↗
PubMedDate not supplied

The role of extraneuronal amine transport systems for the removal of extracellular catecholamines in the rabbit.

As selective inhibitors of the extraneuronal monoamine uptake system (uptake2) suitable for in-vivo studies were not available, the question of whether uptake2 plays a definite role in vivo is largely unresolved. We attempted to resolve the question by using 1,1'-diisopropyl-2,4'-cyanine iodide (disprocynium24), a novel agent that blocks uptake2 in vitro with high potency. Anaesthetized rabbits were infused with 3H-labelled noradrenaline, adrenaline and dopamine, and catecholamine plasma clearances as well as rates of spillover of endogenous catecholamines into plasma were measured before and during treatment with either disprocynium24 or vehicle. Four groups of animals were studied: group I, no further treatment: group II, monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) inhibited; group III, neuronal uptake (uptake1) inhibited; group IV, uptake1 as well as MAO and COMT inhibited. Disprocynium24 (270 nmol kg-1 i.v. followed by an i.v. infusion of 80 nmol kg-1 min-1) did not alter heart rate and mean arterial blood pressure, but increased cardiac output by 22% and decreased the total peripheral vascular resistance by 16% with no difference between groups. When compared with vehicle controls, catecholamine clearances (normalized for the cardiac output of plasma) were decreased and spillover rates increased in response to disprocynium24. Although there were statistically significant between-group differences in baseline clearances (which decreased in the order: group I > group II > group III > group IV), the drug-induced clearance reductions relative to vehicle controls were similar in groups I to IV and amounted to 29-38% for noradrenaline, 22-31% for adrenaline and 16-22% for dopamine. Hence, there was still a significant % reduction in catecholamine clearances even after the combined inhibition of MAO and COMT, and there was no increase in the % reduction of clearances after inhibition of uptake1. Noradrenaline spillover increased in response to disprocynium24 in all four groups by 1.6- to 1.9-fold, whereas a 1.5- to 2.0-fold increase in adrenaline and dopamine spillover was observed in groups II and IV only. The results indicate that disprocynium24 interferes with the removal of circulating catecholamines not only by inhibiting uptake2, but also by inhibiting related organic cation transporters. As disprocynium24 increased the spillover of endogenous catecholamines into plasma even after inhibition of MAO and COMT, organic cation transporters may also be involved in the removal of endogenous catecholamines before they enter the circulation.

Adrenergic Agonists↗
PubMed1981

Projection of ventrolateral medullary (A1) catecholamine neurons toward nucleus tractus solitarii.

The distribution and interconnections of brainstem catecholamine cell groups thought to be important in cardiovascular control were studied using histochemical and ultrastructural techniques in the rabbit. Lesions and microinjections of horseradish peroxidase (HRP) were made in the nucleus tractus solitarii in the dorsomedial medulla, and in the ventrolateral medulla. After lesions of the dorsomedial medulla the fluorescence intensity of the A1-group of catecholamine neurons was increased, and swollen axons could be seen coursing from the ventrolateral medulla toward the lesions on the same side, but not the opposite side. Most of these axons ran in a band about 2 mm in width, centered at the level of the obex. Electron microscopically, specific cells, identified as A1-catecholamine neurons, showed evidence of chromatolysis after the dorsomedial lesions. Following injection of HRP into the nucleus tractus solitarii. A1-catecholamine cells in the ventrolateral medulla on the same side contained the reaction product. Lesions of the ventrolateral medulla did not produce evidence of a reciprocal projection of A2-catecholamine neurons toward the ventrolateral medulla. Thus axons of the A1-group of catecholamine neurons in the ventrolateral medulla project toward the ipsilateral nucleus tractus solitarii in a relatively compact band at the level of the obex. On the other hand, the A2-group of catecholamine neurons in the dorsomedial medulla does not appear to send projections toward the A1-group.

Animals↗
PubMed1994

Catecholamine innervation of the intestine of flying foxes (Pteropus spp.): a substantial supply from enteric neurons.

The distribution of catecholamines in the small and large intestine of flying foxes (Pteropus spp.) was investigated using glyoxylic-acid-induced fluorescence and immunohistochemical staining of tyrosine hydroxylase and dopamine-beta-hydroxylase. Dense networks of varicose axons stained by each of these methods supplied blood vessels, the mucosa and both submucous and myenteric ganglia, but were scarce in the circular and longitudinal muscle. The majority (> 90%) of submucous neuronal perikarya contained both enzymes and most of these also exhibited catecholamine fluorescence. Somata of similar staining characteristics were less common in the myenteric plexus, where single cells were found in only the minority of ganglia. All of the stained submucosal somata and mucosal axons contained vasoactive intestinal peptide, whereas catecholamine-containing axons that supplied the ganglia, external muscle and blood vessels did not. It is concluded that (1) there is dense catecholamine innervation of most tissues in the flying-fox intestine, similar to many other mammals, (2) mucosal axons originate from enteric catecholamine neurons, not found in other mammals, and (3) axons supplying the blood vessels and enteric ganglia are probably of sympathetic origin and can be distinguished from the intrinsic catecholamine-containing axons by their lack of vasoactive intestinal peptide. The roles and interactions of these two types of catecholamine innervation in the control of secretion and motility remain to be identified.

Animals↗
PubMed1980

The effects of acute and chronic administration of morphine on the turnover of brain and adrenal catecholamines in rats.

Brain and adrenal catecholamine turnover in adult female rats treated with morphine was investigated. A different time course response of brain and adrenal catecholamines to alpha-methyl-p-tyrosine methyl-ester (AMT) administration in normal rats was observed; the catecholamine turnover rate in adrenal glands appeared to be much slower than in the brain. Acute morphine increased the turnover of brain dopamine and noradrenaline as well as of adrenal catecholamines, whereas chronic morphine treatment induced a decrease in the turnover of brain noradrenaline. Withdrawal induced by nalorphine produced an increase in the utilization of brain noradrenaline and adrenal catecholamines; this effect could be related to the withdrawl stress situation induced by the opiate antagonist. Although the mechanism of morphine action may implicate other neurotransmitters besides catecholamines, our results contribute to evidence that brain and adrenal catecholamines could be involved in the mechanism of morphine tolerance and/or dependence.

Adrenal Glands↗
PubMed1983

Effects of short-lasting and long-lasting blood pressure changes on the release of endogenous catecholamines in the hypothalamus of the conscious, freely moving rabbit.

In anaesthetized rabbits guide cannulae were stereotaxically inserted into the anterior hypothalamic area and into the posterior hypothalamic nucleus. Additionally, catheters were inserted into the carotid artery and the jugular vein. Some days after the operation push-pull cannulae were inserted through the guide cannulae into the hypothalamic regions of the conscious, freely moving animal. The areas were superfused with artificial CSF and the release of the endogenous catecholamines dopamine, noradrenaline and adrenaline was determined in the superfusates. In the two hypothalamic regions the resting release of the catecholamines rhythmically varied with time at approximately 70 min cycles. A rise in blood pressure induced by the intravenous injection of noradrenaline or tramazoline enhanced the rates of release of the catecholamines in the anterior hypothalamic area. A fall of blood pressure elicited by the intravenous injection of nitroprusside or chlorisondamine decreased the release of the catecholamines in this hypothalamic area. The changes in blood pressure coincided with the changes in the rates of release of the catecholamines in the anterior hypothalamic area. These and previous results concerning changes in the release of endogenous catecholamines in the posterior hypothalamic nucleus also indicate that in the conscious, freely moving rabbit changes in blood pressure lead to counteracting alterations in the release of catecholamines in the two hypothalamic regions.

Animals↗
PubMed1985

The outward transport of catecholamines mediated by uptake2 of the rat heart.

The efflux of 3H-catecholamines from the extra-neuronal tissue of the rat heart was analysed (after inhibition of vesicular and neuronal uptake, monoamine oxidase and catechol-O-methyl transferase). In most experiments, hearts were first loaded with a tracer concentration of a 3H-catecholamine and then washed out. For all four catecholamines [3H-(+/-)-isoprenaline, 3H-(+/-)-adrenaline, 3H-(-)-noradrenaline, and 3H-dopamine] the loading period resulted in virtually the same distribution pattern: most of the radioactivity distributed into "compartment III". However, the rate constants for efflux from compartment III increased in the order 3H-(-)-noradrenaline less than 3H-dopamine less than 3H-(+/-)isoprenaline = 3H-(+/-)-adrenaline. O-methyl-isoprenaline (OMI, a potent inhibitor of uptake2) caused a concentration-dependent and partial inhibition of the efflux of all 3H-catecholamines; its IC50 (half-maximal inhibition of OMI-sensitive efflux) was very close to that for half-maximal inhibition of inward transport by uptake2. It is concluded that there is not only (OMI-resistant) diffusional efflux of 3H-catecholamines, but also (OMI-sensitive) outward transport of 3H-catecholamines. The contribution by each of these processes to total efflux differed considerably from one 3H-catecholamine to the next. U-0521 (the COMT inhibitor used in this study) inhibited the OMI-sensitive efflux of 3H-noradrenaline with an IC50 of about 100 mumol/l. However, no inhibitory effect was found for 10 mumol/l U-0521. During the wash-out period (see above) various unlabelled substrates of uptake2 were added to the perfusion fluid at a concentration equalling 2 X Km.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Multiple calcium channels are required for pituitary adenylate cyclase-activating polypeptide-induced catecholamine secretion from bovine cultured adrenal chromaffin cells.

The effects of L-, N-, P- and Q-type calcium channel antagonists and (+/-)-BayK-8644 on catecholamine release induced by pituitary adenylate cyclase-activating polypeptide (PACAP-27) were investigated in bovine cultured adrenal chromaffin cells. PACAP-27 induced the release of 4-15% of the total cellular catecholamines over 7 min, with an EC50 of 20 nM and the effect approaching maximum at 100 nM. Catecholamine release was fully dependent on the presence of extracellular calcium. The dihydropyridine nitrendipine which inhibits L-type calcium channels inhibited PACAP-27-induced secretion in a concentration dependent manner with an inhibition of 20-30% at 1 microM. In contrast, (+/-)-BayK-8644, which prolongs the opening of L-type calcium channels produced a concentration-dependent increase in PACAP-27-induced catecholamine release with 1 microM increasing release by 40-60%. Blockade of N-type calcium channels with omega-conotoxin GVIA reduced release by 5-15%. Block of P-type channels with low concentrations of omega-agatoxin IVA (< or = 30 nM) had no significant effect on release, while higher concentrations (100-300 nM) which block Q-type channels reduced release by up to 15%. omega-Conotoxin MVIIC, an antagonist of Q-type calcium channels and also of N- and P-type channels, inhibited release in a concentration-dependent manner with a near maximum effect of 30-50% produced by 300 nM. The combination of omega-conotoxin GVIA and omega-agatoxin IVA reduced release by 40-50%. Addition of omega-conotoxin MVIIC (300 nM) to the combination of omega-conotoxin GVIA (10 nM) and omega-agatoxin IVA (100 nM) did not inhibit catecholamine release more than with omega-conotoxin GVIA and omega-agatoxin IVA alone, indicating that 100 nM omega-agatoxin IVA was sufficient to block the Q-type calcium channels. When nitrendipine was used together with omega-conotoxin GVIA, omega-agatoxin IVA and omega-conotoxin MVIIC, catecholamine release induced by 20 nM or 100 nM PACAP-27 was reduced by 70-85%. Taken together these results suggest that influx of calcium through multiple different voltage-sensitive calcium channels mediate PACAP-27-induced catecholamine release from bovine chromaffin cells, and that L-, N- and Q-channels contribute to this response.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1980

Hypertension and propranolol therapy: effect on blood pressure, plasma catecholamines and platelet aggregation.

The effects of propranolol on blood pressure, plasma catecholamine concentration and platelet aggregation were examined in 16 patients with uncomplicated primary hypertension. The patients were studied at rest, during isometric handrip stress and 48 hours after sudden discontinuation of propranolol therapy. Plasma catecholamine concentration and platelet aggregation studies were also carried out in 11 age-matched normotensive and healthy subjects at rest. Plasma catecholamine concentration and platelet aggregation were greater in the hypertensive than in the normotensive subjects, but the difference reached statistical significance for aggregation only. Exercise significantly increased catecholamines and platelet aggregability. The administration of propranolol (240 mg/day) produced a significant decrease in systolic and diastolic blood pressue and in aggregation (the percent of light transmission at 1 microM adenosine diphosphate, at rest) and a significant increase in catecholamine concentration. However, propranolol did not prevent the changes in all these variables with exercise. The abrupt discontinuation of propranolol was not associated with any subjective or objective untoward cardiovascular effect or abnormal changes in plasma catecholamines. However, in some patients the platelet aggregation studies demonstrated a hyperaggregable state, which may be due to a state of supersensitivity of platelets to circulating catecholamines.

Blood Pressure↗
PubMed1984

Inhibition of calcium uptake and catecholamine release by 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) in cultured bovine adrenal chromaffin cells.

Effects of intracellular calcium antagonists, 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) and 1-(5-(p-nitrophenyl)-furfurylidene-amino) hydantoin sodium hydrate (dantrolene sodium), on catecholamine release and 45Ca2+ uptake were studied using cultured bovine adrenal chromaffin cells. TMB-8 inhibited carbamylcholine-evoked catecholamine release and 45Ca2+ uptake in a concentration-dependent manner with a similar potency. On the contrary, dantrolene sodium did not show obvious inhibitory effects of catecholamine release and 45Ca2+ uptake. Although TMB-8 inhibited the high K+-evoked catecholamine release and 45Ca2+ uptake, the potency of the drug was approximately 100-fold less than when used to inhibit the carbamylcholine-evoked catecholamine release and 45Ca2+ uptake. The inhibitory effect of TMB-8 on the carbamylcholine-evoked catecholamine release was not overcome by an increase in an extracellular calcium concentration, and was not due to competitive antagonism at the nicotinic receptor site. Moreover, TMB-8 inhibited the carbamylcholine-stimulated 45Ca2+ efflux, but dantrolene sodium failed to affect it. These results suggest that TMB-8, a well-known intracellular calcium antagonist, prevents the cellular calcium uptake in cultured adrenal chromaffin cells, and thus prevents catecholamine release.

Adrenal Glands↗
PubMed1986

Differential effects of ethanol on plasma catecholamine levels in rats.

Acute ethanol administration (1-4 g/kg, i.p.) had no effect on plasma catecholamine levels in nonstressed animals except at the highest dose where levels of both catecholamines increased. In animals stressed for 30 min, the higher doses had a biphasic effect on plasma catecholamines; at earlier times during stress a reduction in stress-induced increases in both catecholamines was seen, whereas later during stress or after release from stress an increase was noted. Semi-chronic ethanol administration (0.5 and 2 g/kg/day, i.p.) had no significant effect on plasma catecholamine levels in nonstressed rats. In stressed rats, ethanol reduced stress-induced catecholamine increases but these reductions were less than those seen after acute administration. Although ethanol reduced the gross behavioral stress response, no correlation between gross behavioral and biochemical responses was detected. These data show that ethanol can indeed reduce the behavioral and biochemical stress responses in rats but that effects seen depend on the state (nonstressed vs stressed) of the animal, the dose of ethanol (low vs high) used, the length of ethanol administration (acute vs semi-chronic), and the time of measurement of the catecholamine level after ethanol administration.

Animals↗
PubMed1989

Myosin light-chain kinase inhibitor, 1-(5-chlornaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-9), inhibits catecholamine secretion from adrenal chromaffin cells by inhibiting Ca2+ uptake into the cells.

For determination of whether myosin light-chain kinase (MLCK) is involved in the secretory mechanism of adrenal chromaffin cells, the effect of a preferential inhibitor of the enzyme, 1-(5-chlornaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-9), on catecholamine secretion from cultured bovine adrenal chromaffin cells was studied. ML-9 did not affect basal catecholamine secretion, but inhibited catecholamine secretion stimulated by acetylcholine, high K+, veratridine or palytoxin. At similar concentrations to those inhibiting the secretion of catecholamine, ML-9 also inhibited increased [45Ca]2+ uptake by the cells induced by these stimulants. However, it did not inhibit catecholamine secretion induced by the Ca2+ ionophore A23187. Moreover, it did not affect catecholamine secretion from digitonin-permeabilized cells induced by a micromolar Ca2+ concentration in the presence of Mg ATP. These results indicate that ML-9 inhibits catecholamine secretion from adrenal chromaffin cells by inhibiting the transmembrane Ca2+ uptake mechanism, but not by inhibiting the intracellular Ca2+-dependent mechanism. The possible role of MLCK in stimulus-secretion coupling in adrenal chromaffin cells is discussed.

Acetylcholine↗
PubMed1992

Inhibition of nicotinic acetylcholine receptor-mediated secretion and synthesis of catecholamines by sea urchin toxin in cultured bovine adrenal medullary cells.

We previously reported the partial purification and characterization of a toxic substance (sea urchin toxin) isolated from the pedicellariae of the sea urchin Toxopneustes pileolus (Nakagawa and Kimura, Jpn J Pharmacol 32: 966-968, 1982). In the present study, we examined the effect of sea urchin toxin on catecholamine secretion and synthesis in cultured bovine adrenal medullary cells. Sea urchin toxin inhibited the secretion of catecholamines stimulated by carbachol and nicotine but not by veratridine or a high concentration of K+. The toxin inhibited the carbachol-evoked influx of 22Na+ and 45Ca2+ at concentrations similar to those for catecholamine secretion. The inhibition of catecholamine secretion by sea urchin toxin was not overcome by increasing the concentration of carbachol. Preincubation of cells with the toxin caused a time-dependent inhibition in the secretion stimulated by carbachol even when the toxin was removed from the incubation medium. The toxin suppressed catecholamine synthesis and tyrosine hydroxylase activity in carbachol-stimulated cells. In addition, sea urchin toxin inhibited [3H]phencyclidine binding to adrenal medullary cells whereas it did not alter cyclic GMP accumulation caused by muscarine. Further purified fractions from sea urchin toxin by concanavalin A affinity column chromatography also inhibited carbachol-evoked secretion of catecholamines. These results suggest that sea urchin toxin inhibits carbachol-enhanced secretion and synthesis of catecholamines by suppression of nicotinic acetylcholine receptor-mediated Na+ influx and subsequent Ca2+ influx in cultured adrenal medullary cells.

Adrenal Medulla↗
PubMed1994

Effects of the potassium channel openers cromakalim and pinacidil on catecholamine secretion and calcium mobilization in cultured bovine adrenal chromaffin cells.

The effects of two K+ channel openers, cromakalim and pinacidil, on voltage-dependent and receptor-mediated catecholamine secretion and Ca2+ mobilization in bovine adrenal chromaffin cells were studied to determine the role of membrane K+ channels in the regulation of a Ca(2+)-dependent secretory process. Both cromakalim and pinacidil stimulated the efflux of 86Rb (used to monitor K+ permeability) from preloaded cells. Cromakalim and pinacidil did not affect the catecholamine secretion induced by excessive depolarization with 56 mM K+, but inhibited that induced by moderate depolarization with 31 mM K+ in a concentration-dependent manner (1 microM-100 microM). The 31 mM K(+)-induced 45Ca2+ influx and increase in intracellular free Ca2+ concentration [Ca2+]i were also inhibited by these agents at similar concentrations to those for inhibition of catecholamine secretion. Cromakalim and pinacidil inhibited catecholamine secretion, 45Ca2+ influx and increase in [Ca2+]i induced by stimulation of nicotinic acetylcholine (ACh) receptors with carbamylcholine. Furthermore, both cromakalim and pinacidil inhibited the increase in [Ca2+]i induced by carbamylcholine in the absence of extracellular Ca2+, which is thought to be mediated by muscarinic ACh receptors. On the other hand, they did not affect catecholamine secretion induced by Bay-K 8644, Ba2+, A23187, histamine or bradykinin. These results indicate that the K+ channel openers, cromakalim and pinacidil, selectively inhibit catecholamine secretion induced by moderate depolarization or by nicotinic ACh receptor stimulation by inhibiting Ca2+ influx and increase in [Ca2+]i. Furthermore, the results suggest that these K+ channel openers-sensitive membrane K+ channels are involved in the regulation of catecholamine secretion mainly indirectly through effects on the voltage-dependent membrane Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1982

In situ voltammetric microelectrodes: application to the measurement of median eminence catecholamine release during simulated suckling.

Catechol-sensitive microelectrodes (10-30 microns) were developed and then used to study the dynamic regulatory role of the prolactin inhibiting factor, dopamine, under conditions of simulated suckling. Current flow resulting from the electrochemical oxidation of catecholamines at the microelectrode surface was linearly related to the concentration of catecholamines present in solution over the range of 5-100 microM. Endogenous catecholamine levels in the rat median eminence were readily detectable and the electrochemical signal corresponding to dopamine release responded in an appropriate manner to various pharmacologic manipulations. We then implanted carbon microelectrodes into the medial median eminence region among capillaries of the primary portal plexus of urethane anesthetized lactating rats. Catecholamine release into the extracellular fluid was electrochemically measured once each minute before, during and after electrical stimulation (15 Hz, 5-30 V, 15 min) of a surgically isolated mammary nerve trunk. This simulated suckling paradigm reliably evoked prolactin secretory episodes qualitatively similar to those observed during suckling of the nipples by the young. During the period of nerve stimulation, a transient (3-5 min) 65% decline in electrochemically detectable catecholamine release was observed. Following cessation of nerve stimulation an oscillatory pattern of catecholamine release was observed with an overall trend toward an increased level of release. This latter observation corresponds with previous reports of increased hypothalamic dopamine turnover during or following suckling and with the increased levels of dopamine measured in hypophysial portal blood following mammary nerve stimulation. The transient nature of the decline of catecholamine release during the nerve stimulation period may explain why a similar observation has not been forth-coming from experiments utilizing the stalk blood collection technique (unless the standard collection periods are considerably shortened). These observations lead us to reject the hypothesis of a mirror image relationship between stalk blood dopamine and peripheral prolactin levels. Instead, we suggest that a transient decline in dopamine secretion coincident with the onset of suckling acts to prepare the pituitary lactotrophs to respond to a prolactin releasing factor which then facilitates prolactin secretion.

Animals↗
PubMed1986

Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells.

The effects of ketamine, an intravenous anesthetic, on 22Na influx, 45Ca influx and catecholamine secretion were investigated in cultured bovine adrenal medullary cells. Ketamine inhibited carbachol-induced 45Ca influx and catecholamine secretion in a concentration-dependent manner with a similar potency (IC50 40 microM). Ketamine also reduced veratridine-induced 45Ca influx and catecholamine secretion (IC50 260 microM) but did not affect high K-induced 45Ca influx and catecholamine secretion. The influx of 22Na caused by carbachol or by veratridine was suppressed by ketamine with a concentration-inhibition curve similar to that of 45Ca influx and catecholamine secretion. Inhibition by ketamine of the carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines was not reversed by the increased concentrations of carbachol. These observations indicate that ketamine, at clinical concentrations, can inhibit nicotinic receptor-associated ionic channels and that the inhibition of Na influx via the receptor-associated ionic channels is responsible for the inhibition of carbachol-induced Ca influx and catecholamine secretion. At higher concentrations, the anesthetic also inhibits voltage-dependent Na channels but has no effect on voltage-dependent Ca channels.

Adrenal Medulla↗
PubMed1983

Enzymatic deconjugation of catecholamines in human and rat plasma and red blood cell lysate.

We have developed a method for enzymatic hydrolysis of both sulfated and glucuronidated catecholamines in plasma and red blood cell lysate. Hydrolysis occurs in the course of the radioenzymatic assay for catecholamines. In human plasma, catecholamines are conjugated almost entirely with sulfate while, in rat plasma, glucuronides are the main conjugates of epinephrine and dopamine but not norepinephrine. Rat plasma contains less percent conjugated catecholamine than human plasma. Human red blood cell lysate contains less conjugated catecholamine than plasma, whereas free E in lysate exceeds that of plasma and free NE has same level both in sulfated + glucuronidated) catecholamines and the nature of conjugated catecholamines.

Animals↗