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PubMed1980

Inotropic effect of prostacyclin (PGI2) on isolated rat atria at different contraction frequencies.

The effects of a wide range of Prostacyclin (PGI2) concentrations on the Isometric Developed Tension (IDT) of isolated left auricles driven at different frequencies (0.8, 1.6 or 3.3 Hz) were explored. A comparison of the positive inotropism of PGI2, norepinephrine (NE), tyramine and phenylephrine (Phenyl) indicated that PGI2, NE and tyramine enhanced peak tension significantly less at slow (0.8 and 1.6 Hz) than at higher rates (3.3 Hz); whereas Phenyl augmented equally the IDT at all of these three driving frequencies. The positive inotropism evoked by PGI2 was inhibited by (-)-propranolol and also by a treatment with 6-OHDA. Cocaine, normetanephrine and U-0521, augmented the positive inotropic influence of PGI2 on atria paced at a slow rate (0.8 Hz) but not at a faster one (3.3 Hz). These results suggest that the action of PGI2 on atrial contractions is apparently indirect and mediated by the release of tissue catecholamines. In addition the effect of PGI2 and NE at slow and fast rates appears associated with a different relative relevance of the processes which terminate the action of added sympathomimetic agonists, namely, neuronal or extraneuronal uptake as well as metabolization via COMT. These mechanisms seen to be more prominent at slower driving frequencies and could explain the diminished effect of PGI2 and NE on slowly paced atria.

Animals↗
PubMed1976

Inactivation and excretion of dopamine by the cat kidney in vivo.

14C-Dopamine at a dose between 0.16 and 400 nmol per kg body weight was injected locally into the renal artery and urinary excretion of the label was followed for a period of up to 75 min. During the first renal passage the injected kidney excreted 28.2+/-8.3% (n = 8) of the activity applied. As shown by column chromatography the 14C-activity in urine was mainly present as 3,4-dihydroxyphenyl acetic acid (40%), homovanillic acid (15%) and dopamine (app. 20%). Excretion rate and the pattern of dopamine metabolites in urine was independent of the administered dose. Thus, the excretion of dopamine by the cat kidney is linked to an inactivation by the kidney enzymes MAO and COMT. From the literature it is known that in dog and chicken kidney catecholamines are not metabolized to such a large extent during renal excretion.

Animals↗
PubMed1984

The outward transport of axoplasmic noradrenaline induced by a rise of the sodium concentration in the adrenergic nerve endings of the rat vas deferens.

The adrenergic nerve endings of the rat vas deferens were loaded with 3H-(-)-noradrenaline; COMT was inhibited by the presence of 10 mumol/l U-0521, and all experiments were carried out with calcium-free solution. After 100 min of wash-out a neuronal efflux of tritium was obtained which remained constant with time (when expressed as fractional rate of loss; FRL); it contained more DOPEG than noradrenaline. The in vitro administration of reserpine-like drugs (reserpine and Ro 4-1284) increased the FRL of tritium, presumably because of an increase in the leakage of noradrenaline from storage vesicles; the efflux of DOPEG increased more than that of noradrenaline, and the ratio NA/DOPEG declined. Inhibition of the membrane ATPase (by omission of potassium from the medium or by the presence of 3 mmol/l ouabain) increased the FRL of tritium, presumably because of an increase in the net leakage of noradrenaline from the storage vesicles (as a consequence of the fall in the concentration of free axoplasmic noradrenaline; see below). Veratridine also increased the FRL of tritium, partly because of its known reserpine-like effect (Bönisch et al. 1983); in the presence of 1 mumol/l veratridine, the efflux of DOPEG increased. Irrespective of the presence or absence of reserpine or Ro 4-1284, inhibition of the membrane ATPase or the presence of veratridine (agents or procedures which increase the axoplasmic sodium concentration) always resulted in a brisk increase of the efflux of noradrenaline that was accompanied by a simultaneous decrease in the efflux of DOPEG (see above for one exception).(ABSTRACT TRUNCATED AT 250 WORDS)

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1981

Two different biophases for adrenaline released by electrical stimulation or tyramine from the sympathetic nerve endings of the dog saphenous vein.

To study the distribution of alpha- and beta-adrenoceptors dog saphenous vein strips were electrically stimulated (2ms, 30 V, 0.25--20 Hz). The strips either had spontaneous tone (contraction experiments) or were contracted by 0.28 microM prostaglandin F2 alpha in the presence of 7 microM phentolamine (relaxation experiments). In strips without preloading or in strips preloaded with (--)-noradrenaline alpha-adrenoceptor-mediated excitatory responses were readily evoked (contraction experiments) but not beta-adrenoceptor-mediated inhibitory responses (relaxation experiments). In strips preloaded with (--)-adrenaline both alpha-(contraction experiments) and beta-effects (relaxation experiments were readily elicited by electrical stimulation and by tyramine. Thus, strips preloaded with (--)-adrenaline were used to compare alpha- with beta-effects. In these strips the latency between the beginning of the electrical stimulation and the onset of the response was longer for beta- than for alpha-responses. The same applies to responses to exogenous (--)-adrenaline. However, the ratio "latency for beta-/latency for alpha-responses" was 3.6 +/- 0.2 (n = 8) for responses to electrical stimulation and 1.8 +/- 0.1 (n = 12) for responses to (--)-adrenaline (P less than 0.001). Cocaine (12 microM) enhanced the alpha-effect elicited by electrical stimulation 2.8 +/- 0.2 (n = 7) times but did not change the beta-effect, whereas U-0521 (50 microM) enhanced the beta-effect 3.4 +/- 0.2 (n = 8) times without changing the alpha-effect. In strips preloaded with (--)-adrenaline also tyramine caused concentration-dependent beta-responses (relaxation experiments). The concentration of phentolamine and prazosin required to inhibit contractions caused by electrical stimulation were about 5--7 times higher than those required to inhibit contractions caused by exogenous adrenaline or noradrenaline, whereas propranolol was equipotent in reducing beta-responses to adrenaline released by electrical stimulation and to exogenous adrenaline. Our results strongly support the view that alpha-adrenoceptors are in close contract with the nerve endings and beta-adrenoceptors are in close proximity of COMT in a vessel with the nerve endings evenly distributed throughout the media.

Animals↗
PubMed1981

The extraneuronal O-methylation of 3H-(+)isoprenaline by guinea-pig tracheal rings in vitro.

Tracheal rings isolated from male guinea-pigs and incubated in Krebs' solution at 37 degrees C O-methylated 3H-(+/-)-isoprenaline by a saturable, high affinity mechanism. 1. With 3H-isoprenaline at 1 mumol . 1-1, O-methyl 3H-(+/-)isoprenaline (3H-OMI) appeared in the tissue with a half-time for approach to steady state of approximately 10 min and was measured in the incubation medium after about 5 min, its concentration increasing linearly thereafter. With 3H-isoprenaline concentrations ranging from 1 to 200 mumol . 1-1, the total formation of 3H-OMI (estimated from that contained in the tissue and the medium) was maintained at steady state rates for up to 60 min, after initial lag times of between 1 and 3 min. O-methylation obeyed Michaelis-Menten saturation kinetics; Km = 6.14 +/- 0.13 mumol . 1-1, Vmax = 0.31 +/- 0.01 nmol . g-1 . min-1. 2. The catechol-O-methyl transferase (COMT) inhibitor U-O521 and the extraneuronal uptake inhibitor corticosterone both reduced O-methylation of 3H-isoprenaline (0.1 mumol . 1-1) by tracheal rings. However, U-O521 was fully inhibitory (IC50 = 2.6 mumol . 1-1), but corticosterone inhibited by only 46% at concentrations up to 1 mmol . 1-1. 3. The O-methylating activity of the "smooth muscle-rich" component of the trachea was approximately three-times greater than for complete tracheal rings. However, considerable activity was also associated with "cartilage-rich", "smooth muscle-poor" sections. This activity did not seem to be associated with endothelial cells. 4. Histamine strongly inhibited O-methylation (IC50 = 30 mumol . 1-1), but two other contractile agonists, 5-hydroxytryptamine and bethanechol, were weakly active and inactive, respectively.

Animals↗
PubMed1986

The role of co-transported sodium in the effect of indirectly acting sympathomimetic amines.

The adrenergic nerve endings of vasa deferentia of either untreated or reserpine (R) and/or pargyline (P) pretreated rats were loaded with 3H-noradrenaline; COMT was inhibited by U-0521 (U). After 100 min of wash-out with Ca2+-free solution, the efflux of tritium (and of 3H-noradrenaline) from the tissue was largely of neuronal origin and remained constant with time (when expressed as fractional rate of loss; FRL). After 110 min of wash-out the effect of inhibition of the Na+,K+-ATPase (by low K+ or ouabain) on basal and on sympathomimetic amine-induced efflux of tritium (or 3H-noradrenaline, under the condition U) was studied in paired experiments. Inhibition of the Na+,K+-ATPase caused a time-dependent increase in the efflux of tritium (or 3H-noradrenaline) which was inhibited by desipramine. Inhibition of the Na+,K+-ATPase also caused a time-dependent reduction of the initial rate of neuronal uptake of 3H-noradrenaline. The effectiveness of the sympathomimetic amines tyramine and amphetamine in inducing "release" (i.e., outward-transport) of noradrenaline depended on the experimental condition: it was most pronounced under the condition RPU, followed by the condition PU and lowest under the condition U (i.e., in tissue of untreated rats). Inhibition of the Na+,K+-ATPase caused an early and transient enhancement of the "release" of noradrenaline induced by tyramine or amphetamine. This enhancement was seen already within the first min after inhibition of the ATPase, i.e., before a pronounced inhibition of uptake (of noradrenaline) and before a pronounced increase of the basal efflux was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1984

Saturation of monoamine oxidase by intraneuronal noradrenaline accumulation.

After pretreatment of the rats with reserpine and pargyline (to inhibit vesicular uptake and MAO), after an additional in vitro treatment with pargyline, and in the presence of U-0521 (to inhibit COMT), the adrenergic nerve endings of vasa deferentia were loaded with 3H-(-)-noradrenaline by exposure to various concentrations of this amine. Subsequently, tissues were washed out with amine-free solution, and the neuronal efflux of tritium was analysed. During 180 min of wash-out the apparent rate constant for the efflux of tritium decreased with increasing tritium content of the tissue. Prolongation of the wash-out period to 305 min revealed that efflux curves for tritium from heavily loaded tissues became steeper after the 180th min of wash-out. This phenomenon is indicative of saturation (followed by desaturation) of a process that limits the efflux of tritium from heavily loaded tissues. Analysis of the radioactivity of the efflux revealed a characteristic efflux curve for DOPEG: the formation of DOPEG appears to be saturated when the 3H-(-)-noradrenaline content of the tissue is high, in order to become desaturated during prolonged wash-out. These results cannot distinguish between MAO and alcohol dehydrogenase as the saturable enzyme. The formation of the mainly deaminated metabolites (during 60 min of wash-out) was determined in lightly and in heavily loaded tissues. The ratio "formation of metabolites/3H-(-)-noradrenaline content" was lower in heavily than in lightly loaded tissues; the relative decline in DOPEG formation was not accompanied by a compensatory increase in the formation of DOMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The effect of partial inhibition of monoamine oxidase on the steady-state rate of deamination of 3H-catecholamines in two metabolizing systems.

Two different "deaminating systems" were compared (i.e., intact tissues in which an uptake process translocates the 3H-catecholamine from the extracellular space to the intracellular MAO): the adrenergic nerve endings of the rat vas deferens exposed to 10 nmol/l 3H-(-)-noradrenaline, and the extraneuronal deaminating system of the rat heart perfused with 50 nmol/l 3H-(-)-adrenaline. Vesicular uptake and COMT were inhibited. In both systems MAO was partially inhibited by pargyline, and the steady-state tissue content of the 3H-catecholamine was determined as well as the steady-state rate of deamination. Rat vas deferens (preincubated with 10-40 nmol/l pargyline for 30 min). Inhibition of neuronal MAO caused not more than a moderate decrease of the steady-state rate of deamination of 3H-(-)-noradrenaline, but the steady-state tissue content was greatly increased. Determinations of the activity of MAO in homogenates of vasa deferentia showed that preincubation with 10 and 20 nmol/l pargyline inhibited the enzyme by 80 to 95%. Rat heart (of animals pretreated with 1 to 30 mg/kg pargyline). Inhibition of extraneuronal MAO caused a steep decline of the steady-state rate of deamination of 3H-(-)-adrenaline, but only a small rise in the steady-state tissue content. The decisive difference between the two deaminating systems lies in the fact that the ratio "kmao/kout" (where the two k-values characterize the activity of the unsaturated intracellular MAO and the ability of the 3H-catecholamine to leave the relevant cells, respectively) is much higher for the neuronal deaminating system exposed to 3H-(-)-noradrenaline than for the extraneuronal deaminating system exposed to 3H-(-)-adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Neuronal efflux of noradrenaline induced by tris or lithium as substitutes for extracellular sodium.

Vasa deferentia of either untreated or reserpine (R) and/or pargyline (P) pretreated rats were incubated with 3H-noradrenaline and then washed with amine- and Ca2+-free solution until (after 100 min) the efflux of radioactivity largely originated from adrenergic nerve endings; COMT was inhibited by U-0521 (U). After 110 min of wash out, the sodium chloride in the wash-out solution was replaced by an equimolar concentration of either Tris-HCl or LiCl. This caused a desipramine-sensitive (i.e., carrier-mediated) efflux of tritiated noradrenaline. The initial increase of the "low Na+"-induced efflux dependent on the experimental conditions: it was most pronounced when the axoplasmic concentration of noradrenaline was high (RPU) and relatively small when MAO and vesicular storage were intact (U). The effects of Li+ and Tris+ differed with regard to the time course of the efflux of tritium: under all three experimental conditions (RPU, PU, U), Tris+ caused the rate of efflux of tritium to increase gradually within the 30 min period of observation, while Li+ either had a "peak-effect" (RPU, PU) or a "plateau-effect" (U). Under "U-conditions" Tris+ caused a slowly increasing, pronounced increase with time of the efflux of both, 3H-noradrenaline and 3H-DOPEG; whereas Li+ caused only a small and sustained increase of the efflux of 3H-noradrenaline and a decrease in the efflux of 3H-DOPEG.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1983

Accumulation of 3H-(-)noradrenaline in the rabbit aorta not related to uptake1 and uptake2, but sensitive to 3,4-dihydroxy-2-methylpropiophenone (U-0521) and oxytetracycline.

1. Some of the extraneuronal accumulation of 3H-(-)noradrenaline in the rabbit aorta was resistant to uptake2 inhibitors (corticosterone, normetanephrine, phenoxybenzamine). Even combined treatment of the tissue with the competitive inhibitor corticosterone (87 mumol . l-1) and the irreversible inhibitor phenoxybenzamine (90 mumol . l-1) was not more effective than was corticosterone alone. 2. The corticosterone-resistant extraneuronal accumulation of 3H-(-)noradrenaline (0.12 mumol . l-1) was reduced by about 30% by the COMT inhibitor U-0521 (1000 mumol . l-1) and by oxytetracycline (100 mumol . l-1). Combined treatment with U-0521 and oxytetracycline was not more effective than was U-0521 alone. Already 1 mumol . l-1 U-0521 had a half-maximal effect, i.e., it reduced accumulation by 15%. This effect of U-0521 was not related to its known ability to block uptake2. The catechol U-0521 probably inhibited binding of noradrenaline to a catechol-specific site. Furthermore, the accumulation was sensitive to the two iron-chelating agents deferoxamine and phenanthroline but not to ascorbic acid and N-ethylmaleimide. 3. A relatively high formation of 3,4-dihydroxymandelic acid (DOMA) took place in the corticosterone-resistant extraneuronal compartment of the mechanically denervated aorta. This formation of DOMA was probably a consequence of tissue injury brought about by removing the adventitia.

Animals↗
PubMed1983

Autoradiographic study of rat hearts perfused with 3H-isoprenaline.

Bönisch et al. (1974) identified kinetically two extraneuronal compartments into which 3H-isoprenaline distributes in the perfused rat heart: compartment III (characterized by a half time for the efflux of 3H-isoprenaline of about 10 min) had about the same size as compartment IV (half time for efflux: 23 min). These authors suggested that compartment III might be located in the vascular smooth muscle, while compartment IV might be located in myocardial cells. The present study was carried out to validate or refute this suggestion. Rat hearts were perfused for 5, 20 or 60 min with 1 mumol/l 3H-isoprenaline; additional hearts were perfused with 1 mumol/l 3H-isoprenaline for 30 min in the presence of either 20 mumol/l corticosterone or 20 mumol/l corticosterone plus 30 mumol/l cocaine. COMT was inhibited in all experiments (by the presence of 100 mumol/l U-0521). Quantitative autoradiography revealed in all groups that the silver grain density (grains/mm2) was greater over small blood vessels (arterioles and venules) than over myocardial cells. However, total silver grains over myocardial cells greatly exceeded those over small blood vessels (by a factor of 6 to 9). Thus, the suggestion of Bönisch et al. (1974) is untenable. Autoradiographic results obtained with small specimens of ventricular muscle are representative of the whole heart, since "silver grains over total tissue" (per mm2) were highly significantly correlated with the 3H-isoprenaline content of the homogenized hearts (in pmol/g). While corticosterone reduced the accumulation of 3H-isoprenaline in myocardial cells, it failed to affect the appearance of silver grains over Purkinje cells. However, cocaine prevented this type of accumulation. Thus, uptake in Purkinje cells appears to resemble neuronal rather than extraneuronal uptake.

Animals↗
PubMed1980

Monoamines and related enzymes in cerebral cortex and basal ganglia following transient ischemia in gerbils.

The post-ischemic effects on cerebral cortex and basal ganglia monoamine levels and monoamine oxidase (MAO A and B) and catechol-O-methyl transferase (COMT) activities were evaluated in Mongolian gerbils (Meriones unguiculatus) subjected to bilateral common carotid arteries of occlusion for 15 min and reflow for 7 days. Disorders of monoamine metabolism was found in ischemic brain which persisted during the long-term post-ischemia. A rebound increase of norepinephrine and serotonin appeared in early stages (up to 1 h) of post-ischemia both in cerebral cortex and basal ganglia; a rebound increase of dopamine as found only in cerebral cortex. Thereafter, the serotonin level ws enhanced over the control level during the whole post-ischemic period whereas the levels of catecholamines were reduced particularly in basal ganglia. With respect to monoamine content and activities of monoamine degraded enzymes an oscillatory behavior was observed in the post-ischemia. Disorder of the monoamine metabolism found during post-ischemic period possibly contributes to neurological dysfunction after an ischemic insult.

Animals↗
PubMed1985

The saturability of a site of loss and the degree of supersensitivity to agonists which are substrates of this site of loss.

The present investigation was undertaken to test the hypothesis that the experimentally determined degree of supersensitivity to an agonist caused by inhibition of a site of loss depends on the ratio "Km of the site of loss/ED50 of the agonist". The influence of inhibition of neuronal uptake by cocaine on the alpha-adrenoceptor-mediated effect of noradrenaline was studied on the dog saphenous vein; the influence of inhibition of COMT by U-0521 on the beta-adrenoceptor-mediated effect of isoprenaline was studied on the dog saphenous vein and on the guinea-pig trachea; the influence of inhibition of acetylcholinesterase by physostigmine on the effect of acetylcholine was studied on the guinea-pig ileum. To further extend the range of values of the ratio "Km/ED50", several concentrations of phentolamine, propranolol or atropine were used to "increase the ED50" of the respective agonist. It was thus possible to determine the degree of supersensitivity caused by inhibition of a site of loss over a range of "Km/ED50" values of 0.02 to 2,307. In seven situations the ratio "Km/ED50" was higher than 10. In all of these cases the supersensitivity caused by inhibition of the site of loss was maximal. In eleven situations the ratio "Km/ED50" was less than 10 and higher than 0.1 and the supersensitivity obtained was sub-maximal but was closer to the maximum, the closer the ratio was to 10. In two situations the ratio was less than 0.1 and no supersensitivity was obtained. The results confirm the hypothesis.

Acetylcholine↗
PubMed1979

Histofluorescence study on monoamine entry into the brain before and after opening of the blood-brain barrier by various mechanisms.

The relationship between exogenous, circulating monoamines to the wall of cerebral microvessels, and the entrance of these amines into the cerebral parenchyma was studied by the formaldehyde histofluorescence technique in rats. No monoamine fluorescence could be detected in the wall tissue of the microvessels (pericytes and andothelial cells) unless either MAO or COMT were inhibited; these are integral to the blood-brain barrier mechanisms to monoamines. After transient opening of the morphologic blood-brain barrier by either a hypertonic of hypertensive insult, the amine fluorescence in the walls of the microvessels was intensified compared to that which was noted after monoamine oxidase inhibition by itself. Following opening of the structural blood-brain barrier, the circulating amines also passed through into the neuropil where they were concentrated within neurons, as demonstrated by prior depletion of endogenous monoamine transmitters by reserpine. Thus, both enzymatic and morphologic mechanisms in the blood-brain barrier ar involved in impeding the passage of monoamines into the cerebral parenchyma.

Animals↗
PubMed1989

The release of 3H-noradrenaline by p- and m-tyramines and -octopamines, and the effect of deuterium substitution in alpha-position.

The 3H-noradrenaline-releasing effects of p- and m-tyramines and -octopamines, either deuterated or not, were studied in isolated vasa deferentia of the rat (COMT inhibited and calcium-free solution in all experiments). Km for uptake1 was higher for octopamines than for tyramines, but not increased by the introduction of deuterium in alpha-position, except for (probably contaminated) deuterated p-octopamine. Other tissues were preloaded with 3H-noradrenaline. After inhibition of vesicular uptake and MAO equi-releasing concentrations of the eight amines were strictly correlated with Km, they were 6 to 7 times higher for unsubstituted octopamines than for corresponding tyramines. When only MAO (but not vesicular uptake) was inhibited, this difference decreased to about 4-fold, but the releasing potency of the deuterated amines (relative to their parent amines) remained unchanged (except for p-octopamine). When vesicular uptake and MAO were intact, unsubstituted octopamines were only 1.5 to 2.2 times less potent than the corresponding tyramines. Analysis of the efflux of 3H-DOPEG confirmed that this gain in the relative potencies of octopamines is due to their increased ability to mobilize vesicular 3H-noradrenaline; moreover, deuterated amines as well were then better mobilizers than were their parent amines. It is concluded that, provided vesicular uptake is intact, the introduction of a beta-OH-group enhances the ability of indirectly acting sympathomimetic amines to mobilize vesicular noradrenaline; the introduction of deuterium in alpha-position, on the other hand, enhances this mobilizing effect exclusively when MAO is intact.

2-Hydroxyphenethylamine↗
PubMed1986

On the composition and characteristics of microvessels isolated from the rabbit and bovine brain.

Brain capillaries (microvessels) were isolated from the rabbit and bovine brain. Extensive morphological examinations were performed at the light and electron microscopical levels. The relative contribution of endothelium (52%), basal membrane (32%) and pericytes (16%) to the composition of the microvessel was assessed. The ability of the endothelium from bovine brains to maintain a membrane potential, i.e. to accumulate the lipophilic cation [3H]TPMP, was shown. The transmitter catabolizing enzymes MAO and AchE were shown to be, and COMT and GABA-T not to be associated with the microvessel fraction isolated from rabbits.

4-Aminobutyrate Transaminase↗
PubMed1978

Circadian rhythmicity in the methylation of 5-hydroxyindoles and norepinephrine in the pineal gland of 10 day old rats.

In pineals of 10 day old rats 5-hydroxytryptophan, 5-hydroxyindole-3-acetic acid, N-acetylserotonin/5-hydroxytryptophol and norepinephrine are methylated following a circadian rhythm. During the night HIOMT and COMT activities were measured for the above mentioned substrates, while HIOMT activity for 5-hydroxytryptophan and N-acetylserotonin/5-hydroxytryptophol was also determined during daytime.

5-Hydroxytryptophan↗