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At least 91 records · Page 5Linked to original sources
PubMed1981

Influence of sino-aortic baroreceptor denervation on catecholamines, catecholamine-synthesizing enzymes and choline acetyltransferase activity in the brainstem nuclei of the rat.

At one week after sino-aortic baroreceptor denervation in the rat, aortic blood pressure and plasma contents of epinephrine and dopamine beta-hydroxylase (DBH) activity were elevated during resting and conscious states. Stress-induced elevation of blood pressure and plasma epinephrine were markedly pronounced. These changes disappeared at four weeks after denervation. Sino-aortic deafferentation decreased choline acetyltransferase (ChAc) activity in the nucleus tractus solitarii (NTS) and locus coeruleus (LC) and increased DBH activity, norepinephrine levels, phenylethanolamine N-methyltransferase (PNMT) activity and epinephrine levels in the LC, accompanied with a reduction of DBH activity and norepinephrine contents in the nucleus hypothalamicus posterior. These alterations were confirmed one week after denervation but did not persist for a period of four weeks. At four weeks after denervation, ChAc activity was significantly decreased in the nucleus dorsalis nerve of the vagi but not in ;the nucleus ambiguus. During the transient hypertensive phase, sino-aortic deafferentation did not alter DBH and PNMT activities in the NTS, A2 cell and A1 cell areas, and both catecholamine levels in the NTS. In conclusion, sino-aortic denervation transiently decreased ChAc activity in the NTS and LC, and enhanced synthesis and accumulation of norepinephrine and epinephrine in the LC accompanied with a decrease in norepinephrine contents and DBH activity in the nucleus hypothalamicus posterior, causally resulting in short-lasting labile hypertension and activation of the adrenal medulla.

Animals↗
PubMed1980

[A radioreceptor assay for catecholamines. III. A study on the binding sites of catecholamines to alpha-adrenergic receptors (author's transl)].

We established a radioreceptor assay for catecholamines (CA), utilizing the microsomal fraction of bovine myocardium as CA receptors and 3H-norepinephrine (3H-NA) as a ligand. Since 3H-NA binding to the prepared CA binding protein was inhibited by alpha-adrenergic blocking agents, the CA receptors used were assumed to be alpha-adrenergic receptors. In this paper, we studied binding sites of CA to alpha-adrenergic receptors by a displacement study using such compounds as CA, CA metabolites, substances of dihydroxytetrahydronaphthalene derivatives, and other compounds. Various compounds with catechol nucleus had an affinity to the CA binding protein. The displacement study with compounds which were capable of binding to alpha-adrenoceptors had 2 neighbouring phenol groups in the benzenee ring at either position 2 and 3, or at position 3 and 4. On the other hand, either phenylalanine or tyrosine, which has only one phenol group in the benzen ring, did not bind the receptors. It is conceivable, therefore, that the binding sites of CA to alpha-adrenergic receptors is position 2 to 4 of the catechol nucleus, where 2 neighbouring phenol groups exist.

Animals↗
PubMed1986

Thyroid hormone-catecholamine interrelationship during cold acclimation in rats. Compensatory role of catecholamine for altered thyroid states.

Effects of hyper- and hypothyroidism on catecholamine (CA) metabolism in the brain, adrenal glands, liver, and brown adipose tissue (BAT) were studied in adult rats during cold acclimation. Hypothyroidism was induced by the administration of propylthiouracil (PTU) and hyperthyroidism by the injection of thyroxine (T4). After 2 weeks of treatment, they were exposed to cold (5 degrees C) and sacrificed after 1 or 4 weeks. Although the body weight gain of PTU-treated rats were markedly impaired, the body temperature was maintained within normal range. They had increased cerebral dopamine, adrenal CA and BAT norepinephrine (NE) contents, enhanced cerebral tyrosine hydroxylase and adrenal dopamine beta-hydroxylase (DBH) activities and elevated [3H]dihydroalprenolol (DHA) binding to liver plasma membranes (P less than 0.01 vs controls). T4-treated rats showed an increased brain and adrenal CA only after cold exposure. The BAT NE content, DHA binding to liver plasma membranes, and [3H]guanosine diphosphate binding to BAT mitochondria were reduced by 30 to 50% from control values after 4 weeks of cold exposure. These results indicate that during cold acclimation, thyroid hormone deficiency is associated with an accelerated CA synthesis and release, which results in an enhanced BAT thermogenesis, and the hyperthyroid state suppresses CA release, hepatic DHA binding, and BAT heat production. Thus, there is a close metabolic interrelationship between thyroid hormone and CA during exposure to cold. CA appears to ameliorate thyroid hormone excess or deficiency.

Acclimatization↗
PubMed1992

[Excretion of free catecholamines in urine and activity of some enzymes involved in catecholamine metabolism with arterial hypertension during menopause].

This study was performed in 60 women aged between 47-55 years (mean age 50.46 +/- 1.7), divided into two groups: premenopausal and postmenopausal. Each group was subdivided according to arterial pressure: with normal pressure and arterial hypertension. Daily urinary excretion of catecholamines was determined according to method of Euler and Lishajko, the activity of dopamine--beta-hydroxylase in serum according to Nagatsu et al. The activity of catechol-O-methyltransferase in erythrocytes according to Axelrod et al., the activity monoamineoxidase in serum according to Wurtman et al. Daily urinary excretion of vanilmandelic acid determined according to Pisano et al. It was found that women with menopausal arterial hypertension have significantly greater urinary excretion of adrenaline and noradrenaline (p < 0.001) in the premenopausal period, and adrenaline (p < 0.01) in the postmenopausal period. The activity of dopamine-beta-hydroxylase did not differ from the control group. The activity of COMT in erythrocytes of women and MAO in serum of women with menopausal arterial hypertension was significantly lower. Daily urinary excretion of vanillinmandelic acid in women with menopausal arterial hypertension was significantly lower.

Catechol O-Methyltransferase↗
PubMed1991

Distribution of free and conjugated catecholamines between plasma, platelets and erythrocytes: different effects of intravenous and oral catecholamine administrations.

Plasma, platelet and erythrocyte contents of free and conjugated norepinephrine, epinephrine and dopamine were determined by radioenzymatic assay in 12 resting healthy volunteers. Mean platelet/plasma concentration ratios were 533 for free norepinephrine, 502 for free epinephrine and 149 for free dopamine. Corresponding erythrocyte/plasma ratios were 1.04, 1.13 and 4.5, respectively. The presence of conjugated catecholamines in platelets and erythrocytes could be confirmed; however, their relative proportion within these cells, particularly in platelets, was lower than that in plasma. Upon intravenous infusion of dopamine for 3 hr at 5 micrograms kg-1 min-1, concentrations of free dopamine in plasma increased rapidly (280-970-fold), whereas conjugated dopamine only reached maximal values (14-19-fold increase) at 30 to 60 min after cessation of the infusion. The relative distribution of unconjugated dopamine in whole blood between plasma, platelets and erythrocytes changed from mean values of 1:0.33:3.7 at rest to 1:1.1:0.5 at the end of the infusion. As a result of the subsequent rapid decrease of dopamine in plasma and erythrocytes, this distribution was 1:17:1 shortly thereafter and remained constant up to the end of the investigation period. The relative distribution for conjugated dopamine of 1:0.001:0.5 at rest changed to about 1:0.2:0.1 at the termination of the infusion. Oral administration of norepinephrine and dopamine led to increases in the plasma concentrations of these amines in their conjugated forms only, whereas epinephrine concentrations remained constant. These elevations were not accompanied by corresponding increases in platelet and erythrocyte norepinephrine, epinephrine and dopamine contents.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

[Uterine motor responses to catecholamines in the ewe under different steroidal impregnations. Demonstration of the role of endogenous catecholamines].

The electromyographic activity (EMG) of the uterus was recorded in vivo in 6 conscious ovariectomized ewes treated with oestrogen. In 6 cyclic ewes, changes in intrauterine pressure were recorded at the same time as the EMG. Motor responses to noradrenaline, isoprenaline and adrenaline injections were studied at 3 uterine sites in the ovariectomized ewes. Uterine activity was stimulated by noradrenaline and inhibited by isoprenaline, providing evidence that there were both alpha and beta-adrenergic receptors in the myometrium of the oestrogen-treated ovariectomized ewes. Adrenaline caused an increase of myometrial activity at the cervical end and the middle of the uterine horn, demonstrating that alpha-receptors were predominant. Adrenaline had little effect on activity at the tubal end of the horn, but after the administration of propranolol, a blocker of beta-adrenergic receptors, there was a stimulatory effect. These results show that the alpha-receptor/beta-receptors, there was a stimulatory effect. These results show that the alpha-receptor/beta-receptor ratio along the uterine horn was not constant. In cyclic ewes, the effects of noradrenaline and adrenaline in the middle of the uterine horn were stimulatory during oestrus and luteal phase, indicating that alpha-receptors were predominant in that region under both oestrogenic and progesteronic dominance. The perfusion of phentolamine, a blocker of alpha-adrenergic receptors, into ovariectomized ewes treated with oestrogen provided evidence that endogenous catecholamines modulate uterine activity.

Adrenergic alpha-Antagonists↗
PubMed1995

Effect of catecholamine depletion on myocardial infarct size in dogs: role of catecholamines in ischemic preconditioning.

OBJECTIVES: Cardioprotective adaptation to brief periods of ischemia and reperfusion is termed ischemic preconditioning (PC). Limitation of infarct size by preconditioning is associated with marked slowing of ischemic metabolism. The cause of metabolic slowing has not been determined but may involve either pro- or anti-adrenergic mechanisms. Hypothetically, adrenergic stimulation could signal the adaptive response. Alternatively, metabolic slowing during the sustained ischemic challenge could occur through a reduction in beta-adrenergic stimulation. This study was designed to test the role of cardiac norepinephrine (NE) in PC. METHODS: The effect of PC on myocardial infarct size was studied in control dogs and dogs depleted of catecholamines by pretreatment with reserpine (RES; 0.25 mg/kg i.v.). PC was induced by four cycles of 5 min of ischemia and 5 min of reperfusion. Infarcts were produced by 60 min of ischemia and 3 h of reperfusion. Cardiac NE depletion was verified by radioimmunoassay of tissue samples and by absence of hemodynamic response to a tyramine bolus (1.4 mg/kg) administered at the end of each experiment. Infarct size, expressed as percent of area at risk, was controlled for variation in collateral blood flow using analysis of covariance (ANCOVA). RESULTS: Adjusted mean infarct size was 25.5 +/- 3.2% in untreated controls vs. 19.1 +/- 3.3% in RES-treated controls (P = NS). PC limited infarct size in untreated dogs (7.4 +/- 1.8 vs. 25.5 +/- 3.2%; PC vs. control; P < 0.01) but not in RES-treated dogs (15.7 +/- 3.0% vs. 19.1 +/- 3.3%; RES + PC vs. RES; P = NS). Infarct size was larger in dogs with RES + PC than with PC alone, even though there was a trend toward a slight beneficial effect with RES alone. CONCLUSION: The cardioprotective effect of ischemic preconditioning cannot be explained entirely as an anti-adrenergic effect. On the contrary, adrenergic receptor stimulation may be required for the full expression of ischemic preconditioning in canine myocardium.

Adrenergic Uptake Inhibitors↗
PubMed1985

Catecholamine-blocking drugs injected at sites of amine accumulation reverse catecholamine degeneration associated deficits.

It has been hypothesized that catecholamine (CA) accumulation in the axons of degenerating neurons may represent areas of functional neurotransmitter, and may be producing some of the consummatory and locomotory deficits which occur after central CA-depleting lesions. To test this hypothesis further, haloperidol (0.5 microliter of a 7 nM sol.), propranolol (0.5 microliter of a 175 nM sol.) or isotonic saline (0.5 microliter) were injected 1.5 h, 24 h and 48 h after the injection of 6-hydroxydopamine (6-OHDA; 2 microliter of 8 micrograms/microliters) into the lateral hypothalamus (LH) of Sprague-Dawley rats to determine if the hypothermia, motor impairment and consummatory deficits could be reversed. Although haloperidol injection significantly enhanced the hypothermia seen 1.5 h after 6-OHDA injection, open field performance and consummatory responses were significantly improved after haloperidol was injected into the LH where accumulation is known to occur. Three consecutive days of intracerebral haloperidol treatment produced a recovery of body weight regulation lasting for 6 days. Treatment with propranolol enhanced open field performance 1 day after 6-OHDA injection but failed to enhance recovery of consummatory behaviour and body weight control. These results suggest that CA released from areas of accumulation act on adjacent CA receptors to participate in the production of behavioural deficits previously attributed only to the loss of functional neurotransmitter in terminal fields in the forebrain.

Animals↗
PubMed1996

Development of the mesencephalic and diencephalic catecholamine systems in human fetuses: uptake and release of catecholamines in vitro.

Development of catecholamine (CA) systems of the ventral mesencephalon and diencephalon were studied in human fetuses at age 6, 8, 10 and 12 weeks, evaluating the CA specific uptake and K(+)-stimulated release with the isotopic biochemical technique. In the mesencephalon, the [3H]dopamine (DA) uptake was detected as early as 6 weeks, suggesting the existence of either CA neurons or fibers. This was followed by gradual increase of the [3H]DA uptake up to 10 weeks and a subsequent fall at 12 weeks. In the diencephalon, the uptake was first observed at 8 weeks, followed by its decrease at 10 weeks and subsequent increase at 12 weeks. The dynamic uptake is considered as a manifestation of the continuous differentiation of CA neurons and sprouting of CA fibers. In contrast to uptake, no CA release was detected in response to membrane depolarization in the diencephalon and mesencephalon at any age studied, suggesting a timing dissociation between the onset of the CA uptake and K(+)-provoked release in the course of neuron differentiation in human fetuses.

Brain↗