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Michael E Symonds - One of the best experts on this subject based on the ideXlab platform.
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effect of postnatal age and a β3 Adrenergic Agonist zeneca d7114 administration on uncoupling protein 1 abundance in the lamb
Experimental Physiology, 2001Co-Authors: J A Bird, L Clarke, A Mostyn, D T Juniper, Helen Budge, T Stephenson, Michael E SymondsAbstract:We examined the effect of time after birth and beta(3)-Adrenergic Agonist (Zeneca D7114) administration on uncoupling protein-1 (UCP1) abundance and thermoregulation in the lamb. Forty twin lambs, all born normally at term, were maintained at a cold ambient temperature of between 3 and 8 degrees C. At 0.5, 1.75, 5.25, 11.25 and 23.25 h after birth eight sets of twins were fed 20 ml of formula milk +/- 10 mg kg(-1) of beta(3)-Adrenergic Agonist, and 45 min after feeding brown adipose tissue (BAT) was sampled. Colonic temperature was measured and BAT analysed for UCP1 abundance, GDP-binding to mitochondrial protein (i.e. thermogenic activity) and catecholamine content. Colonic temperature declined between 1.25 and 6 h from 40.2 degrees C to 39.2 degrees C and then increased to 39.8 degrees C at 12 h, but increased after feeding at all ages. UCP1 abundance increased from 1.25 h after birth, to peak at 2 h after birth in controls, compared with 6 h after birth in beta(3)-Adrenergic Agonist-treated lambs. The level of GDP-binding to mitochondrial protein did not change significantly with age but was increased by beta(3)-Adrenergic Agonist treatment. The noradrenaline (norepinephrine) content of BAT increased between 1.25 and 12 h after birth, irrespective of beta(3)-Adrenergic Agonist administration. The total weight of perirenal BAT plus its lipid, protein and mitochondrial protein content declined over the first 6 h of life. UCP1 development continues over the first 24 h of neonatal life, and can be manipulated by beta(3)-Adrenergic Agonist administration. This may represent one method of improving thermoregulation in newborn lambs. Experimental Physiology (2001) 86.1, 65-70.
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β2 Agonist ritodrine unlike natural catecholamines activates thermogenesis prematurely in fetal sheep
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1998Co-Authors: John M Bassett, Michael E SymondsAbstract:Prolonged administration of the β2-Adrenergic Agonist ritodrine to fetal sheep increases nonesterified fatty acid mobilization. To investigate whether changes in fetal growth or functional developm...
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effect of β3 Adrenergic Agonist zeneca d7114 on thermoregulation in near term lambs delivered by cesarean section
Pediatric Research, 1996Co-Authors: L Clarke, J A Bird, M A Lomax, Michael E SymondsAbstract:We investigated the effect of a β3-Adrenergic Agonist, Zeneca D7114, on thermoregulation in near-term lambs delivered by cesarean section. Lambs were delivered into a cool ambient temperature of 15°C, and between 60 and 80 min of life were given an oral dose of Zeneca D7114 (10 mg·kg body weight-1) dissolved in 20 mL of milk, or milk alone. During the first 0.5 h of life colonic temperature decreased in all lambs, and then increased to plateau levels (39.6-40.4°C) after 120-150 min of life, in 19 out of 23 lambs studied. In the remaining lambs, colonic temperature failed to return to normothermic values, plateauing at 34.3°C. All control lambs were observed to shiver throughout the study, but after Zeneca D7114 treatment 7 out of 10 normothermic lambs stopped shivering, and plateau colonic temperature was 0.8°C higher. Hypothermic β3-Agonist-treated lambs had significantly lower rates of heat production, breathing frequency, and plasma triiodothyronine and cortisol concentrations than normothermic lambs. The level of GDP binding and norepinephrine content of brown adipose tissue (BAT) sampled from hypothermic β3-Agonist-treated lambs was significantly lower than in normothermic lambs. There was no difference in GDP binding in BAT between control and Zeneca D7114-treated groups, but the Hb content was higher in the latter group. It is concluded that administration of Zeneca D7114 to euthroid lambs enhances their ability to thermoregulate and restore colonic temperature without altering the thermogenic activity of BAT. This response may be mediated by increasing blood flow to BAT and/or an improvement in the animal's thermal efficiency (i.e. decreased heat loss) due to a reduced reliance on shivering thermogenesis.
Susan L Connors - One of the best experts on this subject based on the ideXlab platform.
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in utero beta 2 Adrenergic Agonist exposure and adverse neurophysiologic and behavioral outcomes
American Journal of Obstetrics and Gynecology, 2009Co-Authors: Frank R Witter, Andrew W Zimmerman, James P Reichmann, Susan L ConnorsAbstract:Beta 2 Adrenergic receptor overstimulation during critical periods of prenatal development can induce a permanent shift in the balance of sympathetic-to-parasympathetic tone. This is a biologically plausible mechanism whereby beta 2 Adrenergic Agonists can induce functional and behavioral teratogenesis, which explains their association with increases in autism spectrum disorders, psychiatric disorders, poor cognitive, motor function and school performance, and changes in blood pressure in the offspring. The use of beta 2 Adrenergic Agonists should be limited to proven indications when alternate drugs are ineffective or unavailable; the risks of untreated disease to the mother and fetus are greater than the risk of the beta 2 Adrenergic Agonist.
Juan M. Guerrero - One of the best experts on this subject based on the ideXlab platform.
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β and α Adrenergic mechanisms are involved in regulating type ii thyroxine 5 deiodinase in rat thymus
Life Sciences, 1995Co-Authors: Mohammed Soutto, Juan M. Guerrero, Patrocinio MolineroAbstract:Abstract The role of Adrenergic receptors in regulation of rat thymus type II thyroxine 5′-deiodinase (5′-D) activity was investigated. Our results show that norepinephrine, an α- and β-Adrenergic Agonist elicited an increase in thymus 5′-D activity. Isoproterenol, a β-Adrenergic Agonist, also increased the enzyme activity, being less effective than norepinephrine. Moreover, α-Adrenergic Agonists, i.e., methoxamine, an α 1 -Agonist, and clonidine, an α 2 -Agonist, did not increase 5′-D activity. The effect of isoproterenol was potentiated by methoxamine, but the potentiating effect was observed only at doses of isoproterenol which induce submaximal activation of the enzyme. Administration of propranolol, a β-Adrenergic blocker, and prazosin, an α 1 -Adrenergic blocker, inhibited significantly the activation of the enzyme induced by norepinephrine. However, yohimbine, an α 2 -Adrenergic blocker, had small effect These results show, in hypothyroid rats, a clear regulation by Adrenergic mechanisms of 5′-D activity in the thymus, where α- and β-Adrenergic receptors might be involved.
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β and α Adrenergic receptors are involved in regulating type ii thyroxine 5 deiodinase activity in the rat harderian gland
Life Sciences, 1991Co-Authors: Amalia Rubio, Juan M. Guerrero, M. A. Gonzalez, Miguel A Lopezgonzalez, Carmen OsunaAbstract:The role of alpha- and beta-Adrenergic receptors in regulation of rat Harderian gland type II thyroxine 5'-deiodinase (5'-D) activity was investigated. Our results show that isoproterenol, a beta-Adrenergic Agonist, and phenylephrine, an alpha-Adrenergic Agonist, elicited increases in Harderian gland 5'-D activity. The activation was dependent on the time and the dose of the drug. Other Adrenergic Agonists, i.e., norepinephrine, methoxamine or terbutaline, also clearly increased the enzyme activity. Moreover, administration of propranolol, a beta-Adrenergic blocker, or prazosin, an alpha-Adrenergic blocker, completely prevented the activation of the enzyme induced by norepinephrine. Results show a clear regulation by Adrenergic mechanisms of 5'-D activity in the rat Harderian gland, where alpha- and beta-Adrenergic receptors appear to be involved.
Patrocinio Molinero - One of the best experts on this subject based on the ideXlab platform.
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β and α Adrenergic mechanisms are involved in regulating type ii thyroxine 5 deiodinase in rat thymus
Life Sciences, 1995Co-Authors: Mohammed Soutto, Juan M. Guerrero, Patrocinio MolineroAbstract:Abstract The role of Adrenergic receptors in regulation of rat thymus type II thyroxine 5′-deiodinase (5′-D) activity was investigated. Our results show that norepinephrine, an α- and β-Adrenergic Agonist elicited an increase in thymus 5′-D activity. Isoproterenol, a β-Adrenergic Agonist, also increased the enzyme activity, being less effective than norepinephrine. Moreover, α-Adrenergic Agonists, i.e., methoxamine, an α 1 -Agonist, and clonidine, an α 2 -Agonist, did not increase 5′-D activity. The effect of isoproterenol was potentiated by methoxamine, but the potentiating effect was observed only at doses of isoproterenol which induce submaximal activation of the enzyme. Administration of propranolol, a β-Adrenergic blocker, and prazosin, an α 1 -Adrenergic blocker, inhibited significantly the activation of the enzyme induced by norepinephrine. However, yohimbine, an α 2 -Adrenergic blocker, had small effect These results show, in hypothyroid rats, a clear regulation by Adrenergic mechanisms of 5′-D activity in the thymus, where α- and β-Adrenergic receptors might be involved.
Carmen Osuna - One of the best experts on this subject based on the ideXlab platform.
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β and α Adrenergic receptors are involved in regulating type ii thyroxine 5 deiodinase activity in the rat harderian gland
Life Sciences, 1991Co-Authors: Amalia Rubio, Juan M. Guerrero, M. A. Gonzalez, Miguel A Lopezgonzalez, Carmen OsunaAbstract:The role of alpha- and beta-Adrenergic receptors in regulation of rat Harderian gland type II thyroxine 5'-deiodinase (5'-D) activity was investigated. Our results show that isoproterenol, a beta-Adrenergic Agonist, and phenylephrine, an alpha-Adrenergic Agonist, elicited increases in Harderian gland 5'-D activity. The activation was dependent on the time and the dose of the drug. Other Adrenergic Agonists, i.e., norepinephrine, methoxamine or terbutaline, also clearly increased the enzyme activity. Moreover, administration of propranolol, a beta-Adrenergic blocker, or prazosin, an alpha-Adrenergic blocker, completely prevented the activation of the enzyme induced by norepinephrine. Results show a clear regulation by Adrenergic mechanisms of 5'-D activity in the rat Harderian gland, where alpha- and beta-Adrenergic receptors appear to be involved.