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Biomedical subjects

T Torda

Publications and source records attributed to T Torda.

At least 37 records · Page 2Linked to original sources
PubMed1989

Cholinergic stimulation of phosphoinositide hydrolysis in the rat pineal gland.

Carbachol induced a dose-dependent accumulation of inositol monophosphates in the Wistar rat pineal gland. The relative potency of muscarinic antagonists (atropine greater than pirenzepine much greater than gallamine) in blocking this response suggests the involvement of muscarinic M1 receptors. Following bilateral superior cervical ganglionectomy, the carbachol-induced phosphoinositide response was similar to that seen in sham-operated controls, while adrenergic response was enhanced by 50%. The results indicate that the pineal has functional muscarinic receptors which are not affected by removal of the sympathetic innervation to the gland.

Animals↗
PubMed1989

Characterization of beta 1- and beta 2-adrenoceptor subtypes in the rat sinoatrial node and stellate ganglia by quantitative autoradiography.

We characterized beta-adrenoceptors in rat sinoatrial node (SA) and stellate ganglia by incubating consecutive tissue sections with [125I]iodocyanopindolol, with or without the beta 1-selective (CGP 20712A) or the beta 2-selective (ICI 118,551) antagonists, followed by quantitative autoradiography. In the stellate ganglia, ICI 118,551 displaced more than 90%, and CGP 20712A less than 5%, of the binding sites. CGP 20712A displaced about 50% of the binding sites in the SA, and about 65% in the rat atria. The SA has a high percentage of beta 2-adrenoceptors and the stellate ganglia contains almost exclusively beta 2-adrenoceptor binding sites, implicating beta 2-adrenoceptors in the control of heart rate in the rat.

Animals↗
PubMed1989

Autoradiographic characterization of beta-adrenoceptors in rat heart valve leaflets.

beta-Adrenoceptors were localized and characterized in valve leaflets of the rat heart. Sixteen micrometer-thick tissue sections containing the mitral and aortic valves were incubated with (-)3-[125I]iodocyanopindolol followed by autoradiography with computerized microdensitometry and comparison with 125I-labeled standards. beta-Adrenoceptors were present in all the valves studied. The selective beta 1-adrenoceptor antagonist CGP 20712 A (100 nM) displaced not more than 20% of the total binding sites, suggesting that most of the beta-adrenoceptors in the valve leaflets are of the beta 2-subtype. Forskolin-binding sites were detected in the mitral valve leaflet by incubation of adjacent tissue sections with [12-3H]forskolin. Our results indicate that catecholamines could regulate the function of the heart valves through stimulation of beta 2-adrenoceptors.

Animals↗
PubMed1988

Localization of neuropeptide Y binding sites in the zona glomerulosa of the bovine adrenal gland.

We studied neuropeptide Y (NPY) binding sites in the bovine adrenal gland by incubating tissue sections with [125I]-Bolton Hunter NPY, and then by measuring the number and affinity of binding sites in the tissue with quantitative autoradiography. Specific NPY binding sites were localized exclusively in the zona glomerulosa. These binding sites have an apparent dissociation constant (Kd) of 0.45 +/- 0.06 nM and a binding capacity (Bmax of 134 +/- 15 fmol mg-1 protein. Our results suggest that NPY may directly affect the release of aldosterone in the zona glomerulosa of the adrenal gland.

Animals↗
PubMed1988

Effect of corticosterone treatment and adrenalectomy on phenylethanolamine N-methyltransferase and catecholamines in brain stem and hypothalamic nuclei and superior cervical ganglion of rats.

The effects of corticosterone treatment and adrenalectomy with or without corticosterone replacement on the activity of phenylethanolamine N-methyltransferase (PNMT) and catecholamine content has been studied in isolated brain stem nuclei containing adrenergic and noradrenergic nerve cell bodies, hypothalamic nuclei and in the superior cervical ganglion (SCG) of adult rats. Changes of PNMT activity were found only in a few brain stem areas. In adrenalectomized rats, PNMT activity was decreased in Cl area and in the locus coeruleus, but after corticosterone replacement it returned to the control values. The treatment of rats with corticosterone resulted in a rise of PNMT activity only in C2 area. No significant changes in PNMT activity were seen in the hypothalamic areas in any experimental group of rats. The observed changes of PNMT activity occurred without any measurable changes of noradrenaline (substrate) or adrenaline (product of the reaction catalysed by PNMT). Our results may suggest the involvement of brain stem adrenaline and noradrenaline producing neurons in the central modulation of the pituitary-adrenal function. The basal PNMT activity in SCG of adult rats was very low, but the treatment of rats with high dose of corticosterone or corticosterone replacement to adrenalectomized rats increased PNMT activity in the SCG to the same extent.

Adrenal Glands↗
PubMed1988

3-H-ketanserin (serotonin type 2) binding in the rat frontal cortex: effect of immobilization stress.

The number of 3H-ketanserin (5-HT2) binding sites in rat frontal cortex was estimated in groups of male rats subjected to a single or repeated immobilization stress (IMO). After an acute IMO for 30 or 120 min the number of 5-HT2 binding sites was significantly increased. Similar increase was found even in a group subjected for 120 min IMO for 6 consecutive days and then allowed 24 h rest (i.e. repeatedly stressed controls). If similarly treated animals were subjected to 30 min IMO after 24 h rest, the number of binding sites was increased compared to repeatedly stressed controls, but this was not the case after 120 min IMO. No significant changes of 5-HT2 receptor affinity to 3H-ketanserin were found. The changes of the ratio of 5-hydroxyindolacetic acid/5-hydroxytryptamine were similar to those of binding sites. It was concluded that the enhanced number of cortical 5-HT2 receptor binding sites may result from accelerated serotonin turnover induced by stress, but the results did not indicate any direct association between the serotonin turnover and 5-HT receptor function in the rat frontal cortex.

Animals↗
PubMed1987

Distribution of phenylethanolamine-N-methyltransferase in the rat heart: effect of 6-hydroxydopamine.

The distribution of phenylethanolamine-N-methyltransferase (PNMT), the epinephrine-forming enzyme in the adult rat heart atria and ventricles was studied. The activity of the enzyme in the hearts of adult rats is very low; a significantly higher activity was found in the atria than in the ventricles. A significant increase in PNMT activity was found in all heart areas examined in 6-hydroxydopamine-treated rats compared to vehicle-treated rats. The increased PNMT activity might reflect compensatory or adaptation processes secondary to the destruction of the peripheral sympathetic nerve terminals.

Animals↗
PubMed1987

A radiometric assay for phenylethanolamine N-methyltransferase and catechol O-methyltransferase in a single tissue sample: application to rat hypothalamic nuclei, pineal gland, and heart.

A simple and highly sensitive method for simultaneous assay of phenylethanolamine N-methyltransferase (PNMT) and catechol O-methyltransferase (COMT) is described. These enzymes are determined in a single tissue homogenate using S-[methyl-3H] adenosyl-L-methionine as methyl donor and sequentially incubating with the substrates phenylethanolamine and epinephrine. The radioactive products of the enzymatic reactions, N-methylphenylethanolamine and metanephrine, are extracted and then separated by thin-layer chromatography. The identity of the reaction products has been established chromatographically and the conditions for both enzymatic reactions in the assay procedure have been defined. Measurement of PNMT activity in the rat pineal gland or in minute fragments of other tissues (e.g., brain nuclei) has not been possible using previously described methods. Activities of PNMT and COMT in the rat pineal gland, various hypothalamic nuclei, and the auricular and ventricular myocardia are herein reported.

Animals↗
PubMed1985

Lack of preventive effect of 6-hydroxy-dopamine on a decrease of beta-adrenergic receptors induced by repeated stress in the heart of rats.

Immobilization stress (2.5 h daily) repeated daily for 7 days resulted in a significant decrease in the number of beta-adrenergic receptors in heart compared to control values. Administration of 6-hydroxy-dopamine failed to prevent the stress-induced reduction in the number of beta-adrenergic receptors in the heart of rats as compared to intact stressed rats. These results support the concept that beta-adrenergic receptors in the heart of rats are primarily under the control of the noradrenergic nervous system.

Animals↗
PubMed1985

Effect of repeated immobilization stress on central and peripheral adrenoceptors in rats.

Repeated forced immobilization stress (40 times for 2.5 h daily) reduced the number of beta-receptors in the heart, hypothalamus and brain stem, but not in the spleen of rats. Repeated immobilization stress has also been found to decrease the number of alpha1-receptors in the heart and increase the number of alpha2-receptors in the spleen and brain stem, as compared to control unstressed rats. The number of heart alpha1-, spleen and brain stem alpha2-receptors was still decreased or increased, respectively, 24 h after the 39th immobilization stress. However, at the same time the number of beta-receptors in the heart and brain stem returned to the control levels. We concluded, that the changes in the number of rat adrenoceptors in the heart, hypothalamus and brain stem correlate with peripheral catecholamines released during repeated immobilization stress.

Animals↗
PubMed1983

Pituitary-thyroid function during acute immobilization stress in rats.

In nine experiments a total of 394 male Wistar rats weighing about 300 g was used. In each experiment, one intact control group was used and several other groups were subjected to immobilization (IMO) for 2 to 240 min in a prone position by inserting their heads through steel wire loops fixed on a board and by fasting their limbs to four metal strips by adhesive tape. All animals were killed by decapitation and the levels of thyrotropin (TSH), thyroxine (T4), 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) in plasma were estimated by radioimmunoassay. In one experiment, significant changes in the level of all hormones measured were found within 2 to 15 min of IMO, e.g. an increase of TSH, T4 and rT3 and a decrease of T3. Later (i.e. between 30 and 240 min) the level of TSH, T4 and T3 was repeatedly found to be significantly decreased almost in all experiments as compared to controls. In contrast, a significant increase of rT3 was found only in one out of 7 experiments, the values in other ones being unchanged. Corresponding changes of hormone levels were observed when IMO for 150 min was repeated daily for 7 or 40 days and the animals were sacrificed immediately after the last stress, while one day of rest after such procedures as well as after a single IMO for 150 min appeared to be sufficient for the levels to return to control values.

Animals↗
PubMed1983

Effect of hypophysectomy and administration of TSH on the activity of monoamine oxidase in the thyroid gland of rats.

The thyroid monoamine oxidase (MAO) activity was measured in rats after hypophysectomy and TSH treatment to find out whether the thyroid MAO activity can be modified with TSH. Hypophysectomy decreased MAO activity in the thyroid gland of rats. The administration of TSH (2.5 U kg-1 daily for 5 days) to hypophysectomized rats increased MAO activity and fully compensated the absence of the pituitary. These data suggest that the thyroid gland MAO activity is under the regulatory influence of TSH.

Animals↗
PubMed1983

Effect of adrenal medullectomy on the activity of COMT and MAO in adrenal cortex of control and stressed rats.

The effect of bilateral adrenal medullectomy on the activity of catecholamine degrading enzymes--catechol-o-methyl transferase (COMT) and monoamino oxidase (MAO)--in adrenal cortex and on the level of corticosterone in plasma was studied in the rats subjected either to a single (2.5 h) or repeated (2.5 h daily for 150 days omitting Saturdays and Sundays) immobilization stress. After medullectomy a significant increase of COMT activity was found in adrenal cortex of unstressed controls, while the activity of MAO was significantly decreased. Similar results were observed also in medullectomized animals subjected either to a single or repeated stress. The levels of corticosterone remained unchanged in medullectomized controls, but were significantly decreased in medullectomized and stressed animals. Although the mechanism still remains to be elucidated, these results may be considered as a further contribution to the understanding of the functional interrelations between the adrenal medulla and cortex.

Adrenal Cortex↗
PubMed1982

Changes of plasma and adrenal catecholamines and corticosterone in stressed rats with septal lesions.

The effect of septal lesions on plasma catecholamine and corticosterone (B) levels has been studied in rats during single and 7 times repeated immobilization stress (IMO). Blood samples were obtained via a catheter in the tail artery or by decapitation. The increased circulating epinephrine (EPI) and norepinephrine (NE) levels observed in the initial phase of acute stress as well as the elevated baseline EPI level after six times repeated IMO are indicative of an enhanced response of the sympathetic adrenomedullary system after lesions of the septum. After decapitation of rats with septal lesions there was a significant increase in plasma NE one day after the sixth IMO and a block of EPI increase after the seventh IMO compared to sham-operated rats. The adrenocortical system was similarly found to be activated after septal lesions, exhibiting increased baseline plasma B levels. It has been suggested that the septal region affects the studied systems by exerting an inhibitory tonus. The removal of this inhibitory system results in an increase of adrenocortical and sympathetic-adrenomedullary activities.

Adrenal Glands↗
PubMed1981

Mepacrine treatment prevents immobilization-induced desensitization of beta-adrenergic receptors in rat hypothalamus and brain stem.

Forced immobilization is a severe stress in rats which diminishes levels of epinephrine in specific nuclei in the hypothalamus and brain stem, suggesting that release of epinephrine is stimulated to a rate which exceeds the rate of its replacement. In the pineal gland, frog erythrocytes, C6 astrocytoma cells and rat brain, beta-adrenoceptor agonists appear to regulate the number of their receptors. Exposure to high concentrations of an agonist leads to apparent decrease in receptors reflected by a decrease in maximal specific binding of antagonists. The apparent decreases in receptors have been shown to be attended by decreases in physiologic responsiveness. In C6 astrocytoma cells, beta-agonists stimulate methylation of phosphatidylethanolamine to increase formation of membrane phosphatidylcholine which in turn appears to enhance activation of adenyl cyclase. Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells. In the present study repeated immobilization stress has been found to decrease significantly the number of beta-adrenoceptors in hypothalamus and brain stem while increasing the number of alpha 2-adrenoceptors. The desensitization of beta-adrenoceptors was prevented by treatment with mepacrine.

Animals↗
PubMed1981

Adrenoceptor desensitization after immobilization stress or repeated injection of isoproterenol.

Immobilization stress (2.5 h daily) or repeated injection of isoproterenol (1 mg/kg, 3 times daily) for 1 wk caused a subsensitivity to the chronotropic and pressor effect of epinephrine in pithed rats. Propranolol (1 mg/kg) inhibited, to a greater extent in control than in immobilized rats, the chronotropic effect of epinephrine. The residual heart rates did not differ significantly among control, immobilized, and isoproterenol-treated rats. Practolol (1 mg/kg) but not butoxamine (5 mg/kg) mimicked the effect of propranolol. The subsensitivity in the blood pressure responses was not abolished by injection of either of the beta-adrenoceptor blockers. Butoxamine or propranolol shifted the epinephrine dose-blood pressure response curves to the left. The degree of shift was similar in control and immobilized or isoproterenol-treated rats. Daily injection of quinacrine (16 mg/kg), an antimalarial agent that inhibits phospholipase A2, blocked the subsensitivity to the chronotropic effect of epinephrine, but not that to the pressor effect of epinephrine. These observations suggest that immobilization stress causes desensitization of alpha- and beta 1-receptors but not beta 2-receptors. The mechanism of desensitization of beta 1-receptors by immobilization appears to be similar to that after isoproterenol treatment, possibly due to increased turnover of phospholipids.

Adrenergic beta-Antagonists↗
PubMed1981

Quinacrine-blocked desensitization of adrenoceptors after immobilization stress or repeated injection of isoproterenol in rats.

Repeated forced immobilization or repeated administration of isoproterenol reduces the number of beta adrenoceptors in the heart and spleen of rats. Isoproterenol, but not immobilization, reduced the number of beta receptors in the lung. These changes in beta adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor, although the drug had no effect on beta adrenoceptors when given alone. Immobilization, but not isoproterenol, reduced the number of alpha-1 adrenoceptors in the heart but had no effect on the lung. Quinacrine treatment decreased the number of alpha-1 receptors in heart and lung but increased alpha-2 receptors in the spleen. The changes in receptor number attending exposure to agonists are usually consistent with the expected changes. The effects of quinacrine on such changes suggest that phospholipids are involved in modulating the changes in number of receptors or their availability to interact with ligands.

Animals↗