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PubMed1970

Phase separation in solutions of noradrenaline and adenosine triphosphate: influence of bivalent cations and drugs.

1. From aqueous solutions of biogenic amines, such as noradrenaline plus adenosine triphosphate (ATP), a second liquid phase spontaneously separates in the presence of small amounts of bivalent cations such as calcium. This separation is reversible and temperature-dependent; the concentration of amine and ATP in the bottom phase is several times higher than in the supernatant.2. Analytical ultracentrifugation provides evidence that the second phase consists of high molecular weight aggregates of the amine and ATP.3. The separated second phase of the noradrenaline-ATP system dissolves isothermally on addition of tyramine and amphetamine which in vivo are known to liberate biogenic monoamines and which have a low tendency to aggregate with ATP. The apparent molecular weights of noradrenaline-ATP aggregates are decreased by tyramine and amphetamine. Dopamine does not diminish the second phase and it can also form aggregates of high molecular weight with ATP.4. Bivalent cations in high concentrations diminish or abolish the separation of a second phase.5. Small amounts of reserpine affect phase separation.6. It is concluded that the physico-chemical properties of aggregates of biogenic amines with ATP may be of importance for understanding the storage and release of the amines in vivo.

Adenosine Triphosphate↗
PubMed1971

Cardiovascular reactivity in the experimental hypertensive rat.

1. In pithed preparations, deoxycorticosterone (DOCA)/NaCl-induced hypertensive rats showed increased cardiovascular reactivity to injected noradrenaline, DMPP, tyramine, angiotensin and to sympathetic nerve stimulation.2. Pithed, chronic renal hypertensive rats showed similar hyperreactivity to noradrenaline, DMPP and tyramine but responses to sympathetic nerve stimulation were within normal limits.3. In the isolated, Krebs perfused mesentery preparation, vessels obtained from both DOCA/NaCl and renal hypertensive rats showed hyperreactivity to injected noradrenaline. Responses to periarterial nerve stimulation were also markedly increased in preparations from DOCA/NaCl hypertensive rats, while preparations from renal hypertensive rats showed this effect only at higher rates of stimulation (12 and 25 Hz).

Angiotensin II↗
PubMed1971

Responses of mean arterial pressure to pressor agents and diuretics in renal hypertensive and salt hypertensive rats.

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.

Anesthesia, General↗
PubMed1971

Evidence for inhibition of the reuptake of 5-hydroxytryptamine and noradrenaline by tetrahydronaphthylamine in rat brain.

1. The concentrations of 5-hydroxytryptamine (5-HT), 5-hydroxyindolacetic acid (5-HIAA) and noradrenaline (NA) in homogenized rat brains were determined after intraperitoneal injection of 1,2,3,4-tetrahydro-2-naphthylamine (THN).2. THN caused a decrease in the concentration of brain 5-HIAA without altering its 5-HT content, but the percentage of ;free 5-HT' in the supernatant increased. The decrease in 5-HIAA and the increase in free 5-HT were negatively correlated, suggesting inhibition of the reuptake of 5-HT.3. THN decreased brain NA content without changing free NA. The fact that no increase in free NA occurred is ascribed to the action of catechol-O-methyl-transferase.4. Inhibition of the reuptake of NA and of 5-HT was further studied by using the compounds 5-methyl-alpha-ethyl-meta-tyramine (H 75/12) and 4,alpha-dimethyl-meta-tyramine (H 77/77). The results of these studies also suggested inhibition by THN of the reuptake of 5-HT as well as of NA.5. The action of THN is explained by inhibition of the reuptake of NA and of 5-HT and by release of NA from its stores. However, the possibility is not excluded that, instead of releasing NA from its stores, THN inhibits the enzyme dopamine-beta-hydroxylase.

Animals↗
PubMed1971

Temperature dependence of catecholamine depletion by reserpine in the heart of the toad (Bufo marinus).

1. The catecholamines in toad ventricle were adrenaline (90%) and noradrenaline (10%); there was no dopamine.2. Phenoxybenzamine and tyramine stimulated the isolated heart and reduced the catecholamine content.3. Reserpine treatment of toads kept at 20 degrees C did not affect the adrenaline but reduced the noradrenaline content of the ventricle.4. At 37 degrees C, reserpine caused depletion of both adrenaline and noradrenaline, and the stimulant actions of phenoxybenzamine and tyramine were lost.

Adrenergic Agents↗
PubMed1971

Adrenoceptor functions in the cat choledochoduodenal junction in vitro.

1. The effects of alpha- and beta-adrenoceptor stimulating agents were investigated on three different kinds of preparation of the isolated sphincter of Oddi and on the duodenum of the cat.2. Adrenaline (1.5 x 10(-7)M-6.3 x 10(-7)M), noradrenaline (1.6 x 10(-7)M-6.3 x 10(-7)M), and tyramine (2.9 x 10(-6)M-5.8 x 10(-6)M) increased the activity and tonus of the sphincter musculature and decreased duodenal activity and tone. The effect on the sphincter resulted in increased resistance to flow through the sphincter. The excitatory effects on the sphincter were blocked by phenoxybenzamine (1.7 x 10(-8)M-1.7 x 10(-7)M).3. No effect was produced by tyramine in concentrations up to 4.6 x 10(-5)M on sphincters taken from reserpinized cats. It is suggested that the cat sphincter of Oddi contains adrenergic nerves of functional importance.4. Isoprenaline (1.9 x 10(-8)M-4.7 x 10(-7)M) and terbutaline (3.5 x 10(-7)M-8.8 x 10(-6)M) decreased spontaneous activity and tonus of the sphincter, and diminished resistance to flow through the sphincter. Both agents decreased spontaneous activity and tonus of the duodenum. On a molar basis, isoprenaline was 2-18 times more active than terbutaline on the sphincter and 35-90 times more active on the duodenum. The effects of isoprenaline and terbutaline were blocked by propranolol (3.9 x 10(-7)M).5. It is concluded that the cat sphincter of Oddi contains alpha-adrenoceptors active in contraction of the sphincter, and beta-adrenoceptors active in its relaxation. The beta-adrenoceptors of the sphincter differ from those in the duodenum; it is suggested that they belong to the beta(2)-group (according to Lands' classification).6. The automaticity of the isolated sphincter of Oddi resembled the sphincter activity recorded in vivo and is probably myogenic in nature, as it resisted treatment with phenoxybenzamine (1.7 x 10(-8)M-1.7 x 10(-7)M), atropine (1.4 x 10(-6)M-5.8 x 10(-6)M), hexamethonium (1.4 x 10(-5)M-1.1 x 10(-4)M) and tetrodotoxin (1 mug/ml). The activity of the sphincter has no propulsive function but prevents passage of fluid through the sphincter.

Adrenergic beta-Antagonists↗
PubMed1971

Protection against induction of supersensitivity to catecholamines by cocaine.

1. Adrenaline, noradrenaline, isoprenaline, tyramine, phentolamine, pronethalol, histamine and acetylcholine were each tested for their ability to prevent cocaine from causing supersensitivity to catecholamines in cat spleen strips in vitro. A high concentration of one of these drugs was added to the bath 5 min before cocaine hydrochloride (10 mug/ml). The effect on subsequent responses to catecholamines was compared with the effect of cocaine in control strips in the absence of an interfering drug.2. Phentolamine completely abolished the potentiating effect of cocaine. Large doses of adrenaline or noradrenaline reduced, but did not completely prevent, potentiation. Tyramine, isoprenaline, pronethalol, histamine and acetylcholine did not prevent potentiation.3. The ability of these drugs to interfere with potentiation does not correlate well with their ability to interfere with uptake of noradrenaline. Interference with uptake by cocaine is therefore unlikely to account fully for potentiation.

Acetylcholine↗
PubMed1971

Responses to pressor substances in conscious and anaesthetized cats.

The blood pressure responses to intravenous injections of noradrenaline, tyramine and McN-A-343 have been determined in conscious cats and in cats under pentobarbitone sodium, alpha-chloralose, urethane or alpha-chloralose plus urethane anaesthesia. All four anaesthetic agents reduced the pressor responses, the reduction being most pronounced with urethane and least pronounced with alpha-chloralose. Pentobarbitone sodium exerted a greater inhibitory effect on the responses to McN-A-343 than on those to noradrenaline or tyramine.

Anesthesia, General↗
PubMed1971

Effects of progesterone on cardiovascular responses to amines and to sympathetic stimulation in the pithed rat.

1. Blood pressure and heart rate responses to adrenaline, noradrenaline, tyramine, 5-hydroxytryptamine and stimulation of the spinal sympathetic outflow were measured in pithed rats pretreated either with progesterone (20 mg/kg daily for 14 days) or the vehicle solution of ethyl oleate.2. Pretreatment with progesterone increased the durations but not the magnitudes of the blood pressure and heart rate responses to adrenaline and that phase of the response to sympathetic stimulation attributable to amine release from the adrenal medulla.3. Responses to noradrenaline, tyramine, 5-hydroxytryptamine and that phase of the response to sympathetic stimulation associated with amine release from the sympathetic nerves were not significantly different in the two groups.4. Pyrogallol (5 mg/kg) increased the duration but not the magnitude of responses to adrenaline, noradrenaline and sympathetic stimulation in both experimental groups. The increases in duration were consistently less in animals pretreated with progesterone than in controls.5. Pretreatment with progesterone did not affect the total amount of radioactivity nor the proportion of catechol to non-catechol metabolites excreted in the urine during a period of 7.25 h following an intraperitoneal injection of (+/-) isoprenaline-7-(3)H.6. It is concluded that the effects of progesterone may result from a localized decrease in catechol O-methyl transferase activity within the cardiovascular system.

Animals↗
PubMed1972

Effect of sympathomimetic drugs in eliciting hypertensive responses to reserpine in the rat, after pretreatment with monoamineoxidase inhibitors.

1. The effects of some rapidly metabolized sympathomimetic amines, such as beta-phenylethylamine and p-tyramine, in eliciting hypertensive responses to reserpine in the anaesthetized rat, have been studied.2. Retardation of metabolism, by pretreatment with the monoamineoxidase inhibitors iproniazid or phenelzine, causes beta-phenylethylamine (which in untreated rats has no effect) to induce hypertensive responses to reserpine. Tyramine and other hydroxy substituted phenylethylamines are much less active in this respect, probably because of relatively poor lipid solubility.3. Hypertensive responses to reserpine are due to catecholamine release, which is believed to be from stores made accessible to indirectly acting sympathomimetic amines with high lipid solubility by an action of reserpine on cell membranes.

Animals↗
PubMed1972

A comparison of the pharmacological and biochemical properties of substrate-selective monoamine oxidase inhibitors.

1. M&B 9302, E-250, NSD 2023, and Lilly 51641, substrate-selective inhibitors of monoamine oxidase (MAO), and two non-selective inhibitors of MAO (tranylcypromine and phenelzine) have been compared in the rat for activity in (i) inhibiting rat brain monoamine oxidase in vitro and in vivo using tyramine, 5-hydroxytryptamine (5-HT) and benzylamine as substrates; (ii) increasing brain levels of noradrenaline (NA) and 5-HT and (iii) antagonizing tetrabenazine-induced sedation.2. Concentrations of M&B 9302 and Lilly 51641 required to produce 50% inhibition of 5-HT oxidation by brain mitochondrial MAO were 1.4 x 10(-8)M and 2.5 x 10(-7)M respectively. Higher concentrations were required to inhibit tyramine oxidation whilst benzylamine oxidation was inhibited only at concentrations above 10(-5)M.3. E-250 showed the reverse substrate-selectivity in inhibiting the oxidation of benzylamine at concentrations below that required to inhibit the oxidation of 5-HT. NSD 2023 showed little substrate selectivity in vitro.4. Qualitatively similar results were obtained in vivo, except that NSD 2023 showed more marked substrate-selectivity.5. All the inhibitors except E-250 produced a dose-related rise in brain 5-HT levels. Only phenelzine and Lilly 51641 showed a linear relationship between NA levels and dose.6. All the drugs antagonized, in dose-related fashion, the effects of tetrabenazine in reducing locomotor activity. E-250 and NSD 2023 failed to restore locomotor activity to control levels whilst in high doses the other inhibitors, when given before tetrabenazine, produced a considerable increase in locomotor activity.7. Antagonism of tetrabenazine sedation appears to be correlated with (a) inhibition of the enzyme species that oxidize 5-HT and NA but not with inhibition of the enzyme species that oxidize benzylamine; (b) the rise in brain 5-HT levels rather than NA levels.

Amines↗
PubMed1973

Effect of long-term treatment with high doses of guanethidine on sperm transport and fertility of rats.

1. Male rats treated with guanethidine 25 mg/kg daily for eight weeks had no demonstrable ejaculatory function immediately after cessation of treatment. Four weeks later, ejaculatory function had returned in two-thirds of the males, and after eight weeks, all males were able to deposit sperm in the vagina. However, fertility had returned at that time in only two of the nine males. On the basis of these findings it might be expected that fertility would return in the other males after a more prolonged observation period.2. At autopsy, 66 days after cessation of treatment, the vasa deferentia were congested and filled with viscous material, and along their course dilated regions and pseudocysts containing sperm debris and spermatozoa were found.3. The isolated ducts of the guanethidine-treated males showed a markedly increased response to noradrenaline if compared with ducts from control rats. Response to tyramine was similar in both treated and untreated rats. In view of the increased response to noradrenaline it may be concluded that the noradrenaline stores, which are sensitive to tyramine, were still reduced 66 days after guanethidine treatment had been stopped.

Animals↗
PubMed1973

Monoamine oxidase in rat arteries: evidence for different forms and selective localization.

1. Two forms of monoamine oxidase activity were differentiated in rat mesenteric and femoral artery by means of substrate and inhibitor specificities: one form deaminated tyramine, 5-hydroxytryptamine and noradrenaline and was highly sensitive to pargyline and clorgyline but resistant towards carbonyl reagents. This form resembled type A monoamine oxidase previously described. The other deaminated tyramine but not 5-hydroxytryptamine or noradrenaline and was inhibited by carbonyl reagents but not by clorgyline or pargyline.2. About one third of the total monoamine oxidase in homogenates of rat mesenteric artery was recovered in a 10(5)g supernatant. Both forms were partially soluble, but relatively less of the type A activity was recovered in the soluble fraction.3. Chemical sympathectomy with 6-hydroxydopamine resulted in a loss of 59% of monoamine oxidase activity in the mesenteric artery. There was a selective loss of type A activity, as revealed by the 70% decrease in 5-hydroxytryptamine deaminating ability and by the marked decrease in clorgyline sensitivity. The second monoamine oxidase species was resistant to 6-hydroxydopamine. The soluble activity was not affected by chemical sympathectomy. Most of the transmitter-specific monoamine oxidase of the arterial wall was localized within the adrenergic nerve endings. Our observations are consistent with the hypothesis that extraneuronal monoamine oxidase plays only a minor role in metabolizing noradrenaline in sympathetically innervated tissues.4. Plasma amine oxidase might originate from the arterial wall since it has similar characteristics to that found in the mesenteric artery.

Alkynes↗
PubMed1973

A comparison of the effects of chemical sympathectomy by 6-hydroxydopamine in newborn and adult rats.

1. The effects of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on the cardiovascular system of the rat were compared in, (a) 10-week-old rats treated during the first 14 days after birth with 150 mug/g subcutaneously, and (b) adult rats injected intravenously with 2 x 50 mg/kg on day 1 and 2 x 100 mg/kg on day 7 and the experiments performed on day 8.2. Intravenous administration of 6-OHDA to adult rats almost completely abolished the pressor responses to stimulation of the entire sympathetic outflow in the pithed rat, the contractions of the lower eyelid to stimulation of the cervical sympathetic trunk and the vasconstrictor responses produced by periarterial nerve stimulation of the isolated renal artery preparation. Pressor responses to physostigmine and to tyramine were markedly reduced or abolished in anaesthetized and pithed rat preparations, respectively.3. In corresponding experiments, 10-week-old rats treated as newborns with 6-OHDA showed a marked reduction in the stimulation-induced pressor responses and contractions of the lower eyelid, but completely normal vasoconstrictor responses to periarterial nerve stimulation of the isolated perfused renal artery were obtained. The pressor responses to physostigmine were slightly reduced but the tyramine responses were unchanged.4. Treatment with 6-OHDA at birth caused an almost complete and long-lasting noradrenaline depletion in the heart, spleen, salivary glands and ileum but only a partial depletion in the mesentery from 10-week-old rats. These low noradrenaline levels showed no recovery in rats up to an age of 4 months. The tyrosine hydroxylase activity in both the cervical and stellate ganglia from 10-week-old rats was markedly reduced by treatment with 6-OHDA after birth.5. Injections of 6-OHDA after birth produce an almost complete and permanent sympathectomy of various adrenergically innervated organs in the rat. The vascular system represents a major exception, exhibiting a surprisingly high resistance to this type of chemical adrenergic denervation.

Age Factors↗
PubMed1976

Brain concentrations of biogenic amine metabolites in acutely treated and ethanol-dependent rats.

1 Mass fragmentography was used to measure whole brain concentrations of some of the major metabolites of tyramine, octopamine, dopamine and noradrenaline in acutely treated and in ethanol-dependent rats. 2 Treatments with ethanol, either acutely or chronically, failed to alter significantly brain concentration of p-hydroxphenylacetic and p-hydroxymandelic acid (metabolites derived from tyramine and octopamine respectively). The effect on catecholamine metabolites was marked and therefore suggests that ethanol is selective in its effect on central metabolism of biogenic amines. 3 Acute ethanol treatment significantly increased brain concentration of homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylglycol (MHPG). Vanilmandelic acid (VMA) was not affected. All four metabolites (HVA, DOPAC, MHPG and VMA) were increased in the brains of rats rendered dependent on ethanol while still intoxicated (blood ethanol levels above 200 mg/dl). In ethanol-dependent rats undergoing ethanol withdrawal syndrome (no ethanol present in blood), the brain concentrations of HVA and DOPAC were normal while those of MHPG and VMA continued to be elevated. 4 From the decline in the concentrations of HVA and DOPAC after 50 mg pargyline/kg in control rats and rats acutely treated with ethanol, it was concluded that ethanol has no effect on the transport of phenolic acids across the blood brain barrier. 5 No reversal in the metabolism of catecholamines from an oxidative to a reductive pathway, analogous to that produced by ethanol in the periphery, could be established in the brain. 6 The increase in catecholamine metabolite concentrations after ethanol treatment, either acute or chronic, were interpreted as manifestations of increases catecholamine turnover.

Animals↗
PubMed1977

Fluvoxamine, a specific 5-hydroxytryptamine uptake inhibitor.

1. On the basis of both in vitro and in vivo experiments fluvoxamine has been characterized as a potential anti-depressant drug with almost exclusively 5-hydroxytryptamine (5-HT) uptake inhibiting properties. 2. Fluvoxamine is effective in inhibiting 5-ht uptake by blood platelets and brain synaptosomes. Due to inhibition of the membrane pump the compound prevents 5-HT depletion by the tyramine-derivatives H 75/12 and H 77/77. As a result of the interference with the neuronal re-uptake mechanism for 5-HT, fluvoxamine produces a decreased 5-HT turnover in the brain. Effects of 5-hydroxytryptophan (5-HTP) are potentiated in mice and in combination with pargyline, fluvoxamine induces 5-HT-like behavioural effects. 3. In contrast to tricyclic antidepressants, noradrenaline uptake processes are either unaffected or only slightly inhibited by fluvoxamine. The noradrenaline depleting effects of tyramine derivates are not influenced by fluvoxamine. Reserpine effects, such as ptosis are affected only at very high doses of the test compound. The antagonism by fluvoxamine of the reserpine-induced lowering of the pentamethylenetetrazole convulsive threshold can be regarded as due to an effect upon 5-HT uptake. In contrast to the effects of desmethylimipramine and imipramine, no stimulatory effects are found in rats when rapidly acting reserpine-like compounds are given following a dose of fluvoxamine.

5-Hydroxytryptophan↗
PubMed1979

Effects of verapamil, dantrolene and lanthanum on catecholamine release from rat adrenal medulla.

1. The release of catecholamines (CA) from rat adrenal incubated in vivo in Locke solution was studied. 2. Acetylcholine-induced release of CA and CA release by 56 mM KCl were inhibited by verapamil and lanthanum chloride which block calcium permeability. 3. CA secretion induced by salbutamol or by theophylline was unaffected by either verapamil or lanthanum chloride. 4. Dantrolene-sodium inhibited the CA secretion induced by theophylline but only partially reduced potassium-induced release of CA. 5. Verapamil enhanced the secretion of CA induced by salbutamol (in a calcium-free medium). 6. Tyramine-induced secretion of CA was unaffected by lanthanum chloride, verapamil or dantrolene-sodium. 7. It is suggested that cyclic adenosine 3',5'-monophosphate-mediated CA secretion (induced by theophylline or salbutamol) depends on release of calcium from intracellular stores, and that CA secretion induced by tyramine is independent of intra- or extracellular calcium.

Adrenal Medulla↗
PubMed1980

Responsiveness to vasoactive agents of cerebral and mesenteric arteries isolated from control and reserpine-treated dogs.

1 Pretreatment of dogs for 20 to 24 h before the start of experiments with reserpine (0.5 mg/kg) depleted noradrenaline from cerebral and mesenteric arteries, the diminution being greater in the latter arteries. 2 Contractile responses of helically-cut strips of cerebral and mesenteric arteries to noradrenaline were unaffected by pretreatment with reserpine. Tyramine-induced contractions of mesenteric arteries were markedly attenuated by reserpine-pretreatment, whereas the contraction of cerebral arteries was not influenced. The contractile response of mesenteric arteries to transmural nerve stimulation or nicotine was abolished by reserpine-pretreatment, but the relaxation induced by nicotine of cerebral arteries contracted with prostaglandin F2 alpha was not affected. Pretreatment with reserpine attenuated the contractions of mesenteric arteries induced by angiotensin II, but did not alter the response of cerebral arteries to 5-hydroxytryptamine. 3 In prostaglandin-contracted cerebral and mesenteric arterial strips, relaxant effects of acetylcholine, isoprenaline and K+ were not significantly influenced by reserpine-pretreatment. 4 It appears that tyramine and nicotine do not release noradrenaline from dog cerebral arteries in amounts sufficient to cause significant contractions. Attenuation of the response to angiotensin II by pretreatment with reserpine is not the result of depletion of noradrenaline from the mesenteric arterial wall but may be due to interference with the mechanism specific to actions of angiotensin II.

Acetylcholine↗