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At least 1,459 records · Page 81Linked to original sources
PubMed1978

Competitive antagonism by phentolamine of responses to biogenic amines and the transmitter at a neuroglandular junction.

1. A quantitative study has been made of phentolamine's inhibition of the electrical and secretory responses of the isolated salivary glands of Nauphoeta cinerea Olivier to nerve stimulation and bath applications of agonists. 2. The results suggested that phentolamine is a competitive antagonist having an affinity constant of about 1 micrometer-1 for the receptors for dopamine, noradrenaline, adrenaline and the neurotransmitter. 3. Phentolamine also inhibited responses to 5-hydroxytryptamine in a manner seemingly more complex than competitive antagonism. Attempts to estimate the affinity constant gave values of about 0.08 and 0.015 microgram-1 for inhibition of the secretory and electrical responses respectively. 4. This investigation showed that phentolamine discriminates between two kinds of receptor in this gland, one binding 5-hydroxytryptamine and the other combining with catecholamines and the neurotransmitter.

Animals↗
PubMed1973

Methyltetrahydrofolic acid mediates N- and O-methylation of biogenic amines.

A variety of mammalian and avian tissues N- and O-methylate indoleamines and phenylethylamines, with methyltetrahydrofolic acid as the methyl donor. Because it is considerably more efficient than S-adenosylmethionine, methyltetrahydrofolic acid may be the natural methyl donor in this reaction. With methyltetrahydrofolic acid, serotonin is O-methylated to 5-methoxytryptamine, a novel indoleamine in mammalian brain.

Animals↗
PubMed1974

Biogenic amines and control of melanophore stimulating hormone release.

Release of melanophore stimulating hormone (MSH) from the vertebrate pars intermedia is under inhibitory control by the hypothalamus. Removal of the rat pituitary or the neurointermediate lobe of the frog (Rana pipiens) to in vitro incubation medium results in rapid uninhibited release of MSH. This secretion is inhibited by norepinephrine, epinephrine, phenylephrine, and dopamine, and the inhibition is antagonized by alpha-adrenergic receptor blocking agents. Isoproterenol stimulation of MSH secretion from isolated glands is blocked by pro-pranolol, a beta-adrenergic receptor antagonist. These results implicate dopaminergic or classical alpha-adrenergic receptors (or both) in inhibition of MSH release by catecholamines, and implicate beta-adrenergic receptors in stimulation of MSH release by the bioamines.

Animals↗
PubMed1973

Effect of biogenic amines and cannabinoids on bacterial chemotaxis.

The chemotactic response of Pseudomonas fluorescens was significantly enhanced by the stimulants dl-amphetamine and epinephrine. Acetylcholine, a physiological antagonist of epinephrine, and the cannabinoid tetrahydrocannabinol inhibited bacterial chemotaxis. It may be possible to use bacterial chemotaxis as a bioassay in biochemical studies of drug action.

Acetylcholine↗
PubMed1988

Catabolism of aromatic biogenic amines by Pseudomonas aeruginosa PAO1 via meta cleavage of homoprotocatechuic acid.

Pseudomonas aeruginosa PAO1 catabolized the aromatic amines tyramine and octopamine through 4-hydroxyphenylacetic acid and 3,4-dihydroxyphenylacetic acid (HPA). meta ring cleavage was mediated by 3,4-dihydroxyphenylacetate 2,3-dioxygenase (HPADO), producing 2-hydroxy-5-carboxymethylmuconic semialdehyde (MSA). An NAD-dependent dehydrogenase caused the disappearance of the yellow MSA product, probably forming 2-hydroxy-5-carboxymethylmuconic acid. Induction studies with extracts from mutant cells indicated that the inducer of HPADO was HPA and/or MSA. Strains PAO1.221 (tynC1) and PAO1.303 (tynD1) have chromosomal mutations causing a deficiency in the activity necessary for conversion of 4-hydroxyphenylacetic acid to HPA. Genetic analyses showed that the mutations were in different loci. Strains PAO1.197 (tynE1) and PAO1.185 (tynF1) are deficient in HPADO and the NAD-dependent dehydrogenase, respectively. Plasmid pRO1853 was constructed by cloning approximately 7.3 kilobases of PAO1 chromosomal DNA into the BamHI site of the vector plasmid pRO1614. This recombinant plasmid complemented the tynD1, tynE1, and tynF1 mutations. A putative repressor-binding site involved in the regulation of HPADO synthesis was observed for a subcloned fragment of pRO1853. This recombinant plasmid, pRO1863, failed to complement tynE1 or tynF1 but still complemented tynD1. Another construct, pRO1887, contained 9.2 kilobases of PAO1 chromosomal DNA inserted in the PstI site of the vector pRO1727. Plasmid pRO1887 complemented only the tynC1 mutation. Mapping experiments performed with the chromosome-mobilizing plasmid R68.45 located the mutations described above in a cluster at about 35 to 40 min of the PAO1 chromosome map. The mutations were linked to the proA, thr-48, lys-9015, argF10, and argG markers.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Action of prostaglandin synthetase inhibitors on rostral hypothalamic neurones: thermoregulation and biogenic amines.

Sensitivity of neurones in the rostral hypothalamus of methoxyflurane anesthetized cats to the prostaglandin synthetase inhibitors (PGSIs), salicylate and fenoprofen, has been examined using the technique of microiontophoresis. Results were compared with sensitivity to prostaglandin (PG) E1 and no noradrenaline (NA) and 5-hydroxytryptamine (5HT). Simultaneous applications of PGSIs and NA or 5HT were made to investigate the role of PG in monoamine induced changes in neuronal excitability. PGSIs did not excite these cells, but depression were common, particularly with fenoprofen. PGE1 did not reverse the depressions. NA and 5HT responses were generally unaffected by simultaneous PGSI application and responsiveness to PGSIs was found to be unrelated to amine sensitivity. The results support the conclusion that PGSIs have a depressant action on neurones in this region, which may not be related to inhibition of prostagladin synthesis, and that the actions of microiontophoretically applied NA and 5HT are not dependent upon PG.

Action Potentials↗
PubMed1977

Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors.

The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 3.6.1.3) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.

Adenosine Triphosphatases↗
PubMed1977

Stimulation of cerebral cortical synaptosomal Na-K-ATPase by biogenic amines.

The amines noradrenaline, dopamine, 5-hydroxytryptamine, and histamine (0.01-0.5 mM) enhanced the activity of Na-K-ATPase (EC 3.6.1.3) in rat cerebral cortical synaptosomal fractions. The activities of Mg-ATPase and Ca-Mg-ATPase were not significantly affected. No stimulation of Na-K-ATPase occurred in the presence of chelating agents (0.5 mM EGTA or EDTA) unless 0.5 mM calcium had also been added to the incubation medium. These results are consistent with the hypothesis that amines depress cerebral cortical neurones by activation of an electrogenic sodium pump. Calcium ions appear to be involved in this process.

Adenosine Triphosphatases↗
PubMed1985

The effect of growth hormone on biogenic amines in the hepatic portal circulation of the dog.

The effects of a spike concentration of growth hormone (GH) on hepatic portal and peripheral levels of free serotonin and catecholamines were studied by improved radioenzymatic methods in trained, conscious, normal, adult dogs fitted with an indwelling portal catheter. An injection of ovine GH (6 or 100 micrograms/kg) into a cephalic vein produced in the hepatic portal circulation a transient, statistically significant rise of serotonin and a concomitant significant reduction in the concentration of dopamine, norepinephrine, and epinephrine. No change was found in the peripheral circulation, partly because the amines were conjugated to sulfates and glucuronides and these derivatives are not detectable by our assays. Thus, a pulse of GH not only stimulates the release of pancreatic hormones and glucose turnover, but also affects the portal profile of glucoregulatory bioamines. The present investigation lends further support to our view that the splanchnic area represents an endocrine system whose preferential target is the liver.

Animals↗
PubMed1985

The effect of tryptophan on biogenic amines in the hepatic portal circulation of the dog.

Mongrel dogs were fitted with indwelling hepatic portal catheters. After recovery from surgery, experiments were conducted in fasting, unrestrained, fully conscious, normal dogs which were accustomed to handling and withdrawal of blood samples. L-Tryptophan, a specific serotonin precursor, was injected into a saphenous vein, 10 microM/kg body weight, dissolved in saline. Plasma serotonin, dopamine, norepinephrine, and epinephrine were determined by radioenzymatic assays in blood samples withdrawn at frequent intervals for 2 h, simultaneously from the indwelling catheter and from a catheter temporarily inserted into a saphenous vein other than the one used for the injection of tryptophan. The injection of the amino acid caused a significant elevation of the concentration of platelet-free serotonin within 60 min and this was accompanied by a reduction in the concentration of the catecholamines, dopamine, norepinephrine, and epinephrine. The changes occurred only in the portal circulation and were not detected in peripheral blood samples. The results of these experiments indicate the existence of a cause and effect related interdependence between the splanchnic serotonergic and adrenergic systems in that the tryptophan-stimulated increase in serotonergic activity resulted in a concomitant reduction in gut adrenergic activity.

Animals↗
PubMed1990

A physiological dose of estradiol with progesterone affects striatum biogenic amines.

The acute effect of estradiol and progesterone on dopamine and serotonin metabolism in rat striatum was studied. One subcutaneous injection of 17 beta-estradiol (300 ng) and progesterone (150 micrograms) into intact male rats increased plasma levels of these steroids, while testosterone, corticosterone, and estrone remained unchanged. Dehydroepiandrosterone, androstane-3 beta, 17 beta-diol and dihydrotestosterone remained undetectably low. Prolactin decreased and androstane-3 alpha, 17 beta-diol, and 17-OH progesterone increased, but less than estradiol and progesterone. Peak levels of striatal dopamine, dihydroxyphenylacetic acid, and homovanillic acid were observed 15-45 min after steroid injection with a return to control values after 45-60 min, while serotonin and 5-hydroxyindoleacetic acid levels were slightly decreased. An injection of estradiol (70 ng) with progesterone (70 micrograms) to ovariectomized female rats left plasma prolactin levels unchanged, while striatum dopamine and serotonin as well as their metabolite concentrations peaked 15-60 min after steroid injection and returned to control values after 45-75 min. To allow for a better comparison of the action of these steroids, the effect of estradiol or progesterone alone and in combination on the brain of ovariectomized rats was compared in the same experiment. A similar increase in metabolites of dopamine levels was observed after these steroids alone or in combination, while dopamine levels were increased only after progesterone alone or in combination with estradiol. An injection of estradiol or progesterone to ovariectomized rats led to peak steroid concentrations at approximately the same time in the brain and plasma. In addition, plasma and brain steroid levels were significantly correlated.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗