scholarly journals Bidirectional regulation of Na+,K(+)-ATPase activity by dopamine and an alpha-adrenergic agonist.

1993 ◽  
Vol 90 (1) ◽  
pp. 21-24 ◽  
Author(s):  
F. Ibarra ◽  
A. Aperia ◽  
L. B. Svensson ◽  
A. C. Eklof ◽  
P. Greengard
Keyword(s):  
Atpase Activity ◽  
Adrenergic Agonist ◽  
Bidirectional Regulation ◽  
Alpha Adrenergic Agonist

scholarly journals Mechanisms of L-Triiodothyronine-Induced Inhibition of Synaptosomal Na+-K+-ATPase Activity in Young Adult Rat Brain Cerebral Cortex

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Pradip K. Sarkar ◽  
Avijit Biswas ◽  
Arun K. Ray ◽  
Joseph V. Martin
Keyword(s):  
Cerebral Cortex ◽  
Atpase Activity ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Mammalian Brain ◽  
Neuronal Membrane ◽  
Dependent Manner ◽  
Adrenergic Agonist ◽  
Adult Rat ◽  
Dose Dependent

The role of thyroid hormones (TH) in the normal functioning of adult mammalian brain is unclear. Our studies have identified synaptosomal Na+-K+-ATPase as a TH-responsive physiological parameter in adult rat cerebral cortex. L-triiodothyronine (T3) and L-thyroxine (T4) both inhibited Na+-K+-ATPase activity (but not Mg2+-ATPase activity) in similar dose-dependent fashions, while other metabolites of TH were less effective. Although both T3and theβ-adrenergic agonist isoproterenol inhibited Na+-K+-ATPase activity in cerebrocortical synaptosomes in similar ways, theβ-adrenergic receptor blocker propranolol did not counteract the effect of T3. Instead, propranolol further inhibited Na+-K+-ATPase activity in a dose-dependent manner, suggesting that the effect of T3on synaptosomal Na+-K+-ATPase activity was independent ofβ-adrenergic receptor activation. The effect of T3on synaptosomal Na+-K+-ATPase activity was inhibited by theα2-adrenergic agonist clonidine and by glutamate. Notably, both clonidine and glutamate activateGi-proteins of the membrane second messenger system, suggesting a potential mechanism for the inhibition of the effects of TH. In this paper, we provide support for a nongenomic mechanism of action of TH in a neuronal membrane-related energy-linked process for signal transduction in the adult condition.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

Regulation of Trypanosoma cruzi infectivity by alpha- and beta-adrenergic agonists: desensitization produced by prolonged treatments or increasing agonist concentrations

Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 429-434 ◽  
Author(s):  
A. Ayala ◽  
F. Kierszenbaum
Keyword(s):  
Trypanosoma Cruzi ◽  
Prolonged Exposure ◽  
Inhibitory Effect ◽  
Tissue Level ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Alpha Adrenergic Agonist

SUMMARYWe previously reported that blood forms of Trypanosoma cruzi express alpha- and beta-adrenergic receptors and that binding of specific agonists to these receptors modifies the infective capacity of the parasite in vitro. The present study has revealed that the inhibitory effect of the beta-adrenergic agonist L-isoproterenol and the stimulatory effect of the alpha-adrenergic agonist L-phenylephrine are not produced when the parasite is subjected to prolonged exposure to otherwise effective doses of these agonists or when supraoptimal doses of these agonists are used. We refer to these phenomena as ‘desensitization’ because of their analogy with vertebrate cells becoming desensitized by prolonged exposure to, or relatively high concentrations of, adrenergic agonists. At a constant agonist concentration, T. cruzi desensitization was time-dependent and, when the time of parasite treatment with the agonists was not changed, the higher concentrations of the agonist tested were the most effective in producing desensitization. The reduced infectivity resulting from treatment with optimal doses of L-isoproterenol was accompanied by elevated levels of cyclic adenosine mono- phosphate (cAMP) which were not detectable when L-isoproterenol concentrations producing desensitization were used. This finding implicated cAMP as a likely second signal in the inhibitory mechanisms of this agonist. No significant change in cAMP was detectable in parasites treated with L-phenylephrine, leaving open the question about how optimal doses of this alpha-adrenergic agonist enhance T. cruzi infectivity. Parasite responsiveness to alpha- and beta-adrenergic agonists as well as the desensitization effects define a system which regulates infectivity and could be modified at the host tissue level by naturally occurring agonists.

scholarly journals Phosphatidic acid and arachidonic acid each interact synergistically with glucagon to stimulate Ca2+ influx in the perfused rat liver

1987 ◽  
Vol 247 (3) ◽  
pp. 613-619 ◽  
Author(s):  
J G Altin ◽  
F L Bygrave
Keyword(s):  
Arachidonic Acid ◽  
Phosphatidic Acid ◽  
Synergistic Action ◽  
Perfused Rat Liver ◽  
O2 Uptake ◽  
Adrenergic Agonist ◽  
Glucose Output ◽  
Rat Livers ◽  
Alpha Adrenergic Agonist ◽  
Stimulation Of

The administration of phosphatidic acid to rat livers perfused with media containing either 1.3 mM- or 10 microM-Ca2+ was followed by a stimulation of Ca2+ efflux, O2 uptake and glucose output. The responses elicited by 100 microM-phosphatidic acid were similar to those induced by the alpha-adrenergic agonist phenylephrine. Contrary to suggestions that phosphatidic acid acts like a Ca2+-ionophore, no net influx of Ca2+ was detected until the phosphatidic acid was removed. Sequential infusions of phenylephrine and phosphatidic acid indicate that the two agents release Ca2+ from the same intracellular source. The co-administration of glucagon (or cyclic AMP) and phosphatidic acid, and also of glucagon and arachidonic acid, led to a synergistic stimulation of Ca2+ uptake of the liver, a feature similar to that observed after the co-administration of glucagon and other Ca2+-mobilizing hormones [Altin & Bygrave (1986) Biochem. J. 238, 653-661]. A notable difference, however, is that the synergistic stimulation of Ca2+ uptake induced by the co-administration of glucagon and arachidonic acid was inhibited by indomethacin, whereas that induced by glucagon and phosphatidic acid, or glucagon and other Ca2+-mobilizing agents, was not. The results suggest that the synergistic action of glucagon and arachidonic acid in stimulating Ca2+ influx is mediated by prostanoids, but that of glucagon and phosphatidic acid is evoked by a mechanism similar to that of Ca2+-mobilizing agents.

An alpha-adrenergic agonist protects hearts by inducing Akt1-mediated autophagy

2015 ◽  
Vol 456 (1) ◽  
pp. 250-256 ◽  
Author(s):  
Mikihiko Nakaoka ◽  
Eri Iwai-Kanai ◽  
Maki Katamura ◽  
Yoshifumi Okawa ◽  
Yuichiro Mita ◽  
...  
Keyword(s):  
Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

scholarly journals The α-adrenergic-mediated activation of Ca2+ influx into cardiac mitochondria. A possible mechanism for the regulation of intramitochondrial free CA2+

1981 ◽  
Vol 200 (2) ◽  
pp. 379-388 ◽  
Author(s):  
P Kessar ◽  
M Crompton
Keyword(s):  
Steady State ◽  
Isolated Heart ◽  
Cardiac Mitochondria ◽  
Adrenergic Agonist ◽  
Adrenergic Regulation ◽  
Simultaneous Measurements ◽  
Rat Hearts ◽  
Oxoglutarate Dehydrogenase ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

Mitochondria isolated from rat hearts perfused with adrenaline, and from hearts excised from adrenaline-treated rats, showed an enhanced rate of respiration-dependent Ca2+ uptake. Adrenaline pretreatment did not change the activity of the Na+/Ca2+-antiporter of isolated heart mitochondria. Simultaneous measurements of the membrane potential revealed that perfusion with adrenaline has no significant effect on this parameter during Ca2+ accumulation. The activation of Ca2+ uptake was induced also by the alpha-adrenergic agonist, methoxamine, but not by the beta-adrenergic agonist, isoprenaline. Methoxamine pretreatment also increased the sensitivity of alpha-oxoglutarate dehydrogenase in intact mitochondria to 10 nM--300 nM extramitochondrial Ca2+ during steady-state Ca2+ recycling across the inner membrane. Possible implications of these data for the adrenergic regulation of oxidative metabolism are discussed.

Calcineurin-GATA4 pathway is involved in alpha-adrenergic agonist-mediated protection against myocardial cell apoptosis

1999 ◽  
Vol 5 (3) ◽  
pp. 22
Author(s):  
Koji Hasegawa ◽  
Tsuyoshi Kakita ◽  
Eri Iwai-Kanai ◽  
Tatsuya Morimoto ◽  
Shigetake Sasayama
Keyword(s):  
Cell Apoptosis ◽  
Myocardial Cell ◽  
Adrenergic Agonist ◽  
Alpha Adrenergic Agonist
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