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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In white rats both adapted and unadapted to cold, the RQ dynamics during cold exposure, noradrenaline and ganglion blocking agent administration, were studied. The adapted animals' RQ in thermoneutral conditions was shown to be a little higher than in the control rats; 0.5 mg/kg noradrenaline injections induced a clear RQ decrease in the former and did not influence the latters' RQ. Cold exposure was followed by a RQ decrease in both. Ganglion blocking agent administration decreased the RQ in the adapted animals and prevented it from falling in the control those. Noradrenaline is supposed to be the main but not the only factor activating lipolysis in the cold adapted animals.
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PMID:[Mechanisms of the thermogenic action of noradrenaline during adaptation to cold]. 0 Feb 57

When rats were exposed to immobilized cold stress, adrenaline content in the adrenal gland as well as noradrenaline content in the brain stem were reduced drastically, while noradrenaline content in the atria was not altered by the application of stress. Oral administrations of taurine (4-7 g/kg/day, for 3 days) prevented the stress-induced decline of adrenaline in the adrenal gland and this preventive effect could not be duplicated by the administration of L-isoleucine or DL-methionine. In hypophysectomized rats, the stress also induced a significant fall in adrenaline content of the adrenal gland, however taurine administration did not show significant preventive effects on the decline in adrenal catecholamines. The immobilized cold stress induced a significant increase in blood sugar and this increase was antagonized by pretreatment with taurine. Taurine had no significant effects on the stress-induced increase in the activity of adrenal tyrosine hydroxylase and the turnover rate of adrenaline in the adrenal gland measured by the rate of decline of this amine following alpha-methyl-tyrosine administration. The administration of taurine, in both in vivo and in vitro, inhibited the release of adrenaline from adrenal medullary granules, but that of dopamine-beta-hydroxylase was not significantly affected. The stress-induced elevation of the blood level of corticosterone was not affected by taurine administration. These findings indicate that taurine antagonizes the stress-induced elevation of blood sugar by reducing adrenaline output from the adrenal gland. The regulatory mechanism most likly involves the inhibition of adrenaline release from adrenal medullary granules, possibly by stabilizing the membrane of the granules.
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PMID:Effect of taurine on alteration in adrenal functions induced by stress. 0 14

Norepinephrine turnover rates and tyrosine hydroxylase activities were determined in the interscapular brown fat pad of the rat during cold acclimation, hyperthyroxinism, and after thyroidectomy. Rats were cold acclimated by placement in a cold room, one rat to a cage, for a period of 6 wk. Hyperthyroxinism was induced by daily subcutaneous injections of L-thyroxine (1 mg/kg) for 6 days. Norepinephrine turnover rate and enzyme activity were determined at the end of each experimental period and at 8 wk after thyroidectomy. The rate of norepinephrine turnover increased during cold acclimation and hyperthyroxinism and decreased after thyroidectomy. Cold acclimation resulted in a significant increase in tyrosine hydroxylase activity, whereas no significant effect on enzyme activity was observed in hyperthyroxinism or after thyroidectomy. None of the conditions produced a change compared to controls in the apparent Km of tyrosine hydroxylase for L-tyrosine. Cold acclimation resulted in a significant decrease in the apparent Km of tyrosine hydroxylase for pterin cofactor, whereas thyroxine treatment and thyroidectomy had no effect.
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PMID:Thyroid cold acclimation influences on norepinephrine metabolism in brown fat. 1 13

1 Intravenously administered phentolamine provoked immediate decreases in diastolic blood pressure but increases in heart rate and cardiac output. 2 These immediate circulatory effects had largely disappeared twenty minutes after administration and at this time phentolamine did not inhibit increases in blood pressure which were provoked during hand immersion in ice-cold water. 3 Log dose-response curves of noradrenaline induced increases in systolic and diastolic pressure 20 min after intravenous phentolamine were shifted to the right in a parallel manner compared with the curves before phentolamine administration. 4 It was concluded that the immediate and short acting effects induced by phentolamine are due to a non-specific vasodilator effect but in addition phentolamine causes a longer acting alpha-adrenoceptor blockade at vascular adrenoceptor sites. However, by producing both pre- and post-synaptic alpha-adrenoceptor blockade this may explain why this drug exerts only a weak antihypertensive effect.
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PMID:Circulatory and alpha-adrenoceptor blocking effects of phentolamine. 2 72

The cellular localization of the enzymes tyrosine hydroxylase (TH), aromatic amino-acid decarboxylase (or dopa decarboxylase, DDC), dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) in the adrenal medulla of adult rats and rat fetuses (14th, 17th, 18th, 19th and 21st day) was examined. In the prenatal stages the medullary blastema and an adjacent part of the primitive sympathetic trunk were also investigated. Tissues were fixed in ice-cold 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.2). Cryostat sections (10 micron in thickness) were stained by the indirect immunofluorescence technique. Rabbit antibodies to TH (isolated from human pheochromocytoma), DDC, DBH and PNMT (the latter three isolated from bovine adrenal medulla) were used. Sections incubated with serum of non-immunized rabbits were used as controls. In the adult adrenal medulla, two cell types can be distinguished. One cell type contains only TH, DDC and DBH. The other cell type contains PNMT in addition. It is concluded that these cells correspond to the noradrenaline-(NA-) and adrenaline- (A-)storing cells respectively. In all prenatal stages TH, DDC and DBH are found in the primitive sympathetic trunk, in the medullary blastema, and in the medullary cells which have migrated into the cortical "anlage". PNMT is observed for the first time on the 18th day. Moreover, PNMT could only be demonstrated inside the adrenal gland. From these observations it is concluded that the capacity to synthesize NA is developed even before the "medullary" cells have reached the cortical "anlage". On the contrary, the capacity to synthesize A seems to be acquired only after this contact is established. The hypothesis is put forward that this phenomenon might indicate the induction of PNMT by glucocorticoids secreted by the fetal cortex.
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PMID:Appearance of tyrosine hydroxylase, aromatic amino-acid decarboxylase, dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase during the ontogenesis of the adrenal medulla: an immunohistochemical study in the rat. 4 Jul

The effect of graded doses of drugs modifying adrenergic activity on basal and cold-stimulated TSH secretion was studied in male rats. alpha-methyl-p-tyrosine (aMPT) (16 h before 30 min cold-exposure), phenoxybenzamine (1 h), Ca-fusarate (1 h) and diethyldithiocarbamate (DDC) (1 and 18 h) dose-dependently depressed the cold-stimulated TSH secretion. The effect of reserpine (24 h) was not significant. Clonidine (1 h), dihydroxyphenyl-serine (DOPS) (1 h), noradrenaline (NA) (1 h), and L-Dopa (1 h) were also effective in decreasing serum TSH levels, but dopamine (DA) (ad 2 mg/kg, 1 h) had no effect. Basal TSH levels were also decreased by various doses of clonidine, DOPS and NA, given ip 1 h before sacrifice. Clonidine (1 mg/kg), NA (1 mg/kg), DA (2 mg/kg), aMPT (300 mg/kg), phenoxybenzamine (2 or 20 mg/kg), Ca-fusarate (50 mg/kg) or L-Dopa (200 mg/kg) did not modify the TRH-induced TSH response. These results cannot be explained by assuming only a stimulatory function for the adrenergic system on the secretion of TSH in the rat. The site of the possible inhibitory function of noradrenaline in the control of TSH cannot be deduced from these results, but various possibilities are discussed.
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PMID:Dual action of adrenergic system on the regulation of thyrotrophin secretion in the male rat. 10 32

The calorigenic effect of infused adrenaline and noradrenaline was measured in cold-acclimated rats. The slopes of the dose-response curves for the two catecholamines and the maxima of the curves were the same. The adrenaline dose-response curve showed a shift to the right, towards higher infusion doses, compared with the noradrenaline curve. Thermogenesis due to the two catecholamines was not additive throughout the whole range of doses used. In interaction with noradrenaline, propranolol caused a parallel shift of the dose-response curve to the right, whereas in interaction with adrenaline it depressed the maximum. The concept that the two catecholamines act via different regulation sites on a common thermogenetic effector is discussed.
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PMID:Substitution of calorigenic effects of noradrenaline and adrenaline and differences in their inhibition by propranolol. 13 58

Presynaptic inhibition of the extensor (quadriceps, QUAD) monosynaptic reflex (MSR) in unanaesthetized decerebrate cats was antagonized by imipramine hydrochloride (2-5 mg/kg), 5-hydroxytryptophan (75 mg/kg) and a specific 5-hydroxytryptamine (5-HT) neuronal uptake blocker, fluoxetine hydrochloride (Lilly 110140, 0.25-6 mg/kg). These effects of imipramine and fluoxetine were partially reversed by the 5-HT antagonist, cyproheptadine hydrochloride (5 mg/kg), and completely reversed by the application of a thoracic cold block which prevents supraspinal inputs to the caudal spinal cord. Imipramine, however, failed to antagonize this inhibition in animals pretreated with either DL-p-chlorophenylalanine (p-CPA, 300 mg/kg i.p. for 2 consecutive days) or DL-a-methyl-p-tyrosine methyl ester hydrochloride (a-MPt, 125 mg/kg i.p. 16 and 4 h prior to the experiment). Cyproheptadine (2.5--5 mg/kg); phenoxybenzamine hydrochloride (2.5-5 mg/kg) and a cold block enhanced the inhibition of this extensor MSR but a cold block failed to alter the inhibition in animals pretreated with p-CPA or a-MPT. Presynaptic inhibition of the flexor (posterior biceps-semitendinosus, PBST) MSR was however not blocked by imipramine, fluoxetine or a cold block nor enhanced by cyproheptadine or phenoxybenzamine. The effects of the drugs tested and a cold block on the excitability of the QUAD group Ia afferents were reciprocal to those on the MSR during presynaptic inhibition. The results of this study indicate that descending tonically active systems (1) involving 5-HT and noradrenaline, antagonize presynaptic inhibition of the QUAD but not the PBST-MSR, (2) decrease the excitability of the QUAD Ia afferents and (3) increase the excitability of QUAD motoneurones.
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PMID:Tonic inhibitory influence of a supraspinal monoaminergic system on presynaptic inhibition of an extensor monosynaptic reflex. 13 93

Total metabolism, body temperature and basic circulatory parameters (the heart rate, blood pressure, blood oxygen content and hind limb blood flow) were measured in anaesthetized cold-acclimated male laboratory rats exposed to the calorigenic action of noradrenaline. In addition, cardiac output, the oxygen extraction coefficient and peripheral vascular resistance were calculated from these data.
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PMID:Effect of intravenously infused noradrenaline on the cardiovascular system of cold-acclimated rats. 14 22

Rats treated with ACTH and hydrocortisone for 4 weeks were infused i.v. with noradrenaline or exposed to cold at -15 degrees C for 2 hours, and changes in the rectal temperature and plasma concentrations of NEFA, sugar, and lactate were observed. Rats received single injection of ACTH and hydrocortisone, warm- and cold-acclimated rats were used as controls. In ACTH- and hydrocortisone-treated rats, the noradrenaline infusion caused a significant elevation of the rectal temperature, but lowering of the rectal temperature induced by the acute cold exposure in these treated rats did not differ from the changes in control groups. Moreover, considerable differences were found between these treated rats and cold-acclimated ones in plasma concentrations of NEFA, sugar and lactate after noradrenaline infusion and acute cold exposure. From the results it was inferred that chronic treatment with ACTH and hydrocortisone did not produce similar adaptive metabolic alterations to those found in the course of cold acclimation.
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PMID:[Sensitivity to noradrenaline and cold tolerance of rats treated chronically with ACTH and adrenocortical hormone (author's transl)]. 16 34


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