Antidipsogenic effects of central adenosine-5'-triphosphate

Besides other physiological functions, adenosine-5'-triphosphate (ATP) is also a neurotransmitter that acts on purinergic receptors. In spite of the presence of purinergic receptors in forebrain areas involved with fluid-electrolyte balance, the effect of ATP on water intake has not been investigated. Therefore, we studied the effects of intracerebroventricular (icv) injections of ATP (100, 200 and 300 nmol/µL) alone or combined with DPCPX or PPADS (P1 and P2 purinergic antagonists, respectively, 25 nmol/µL) on water intake induced by water deprivation. In addition, the effect of icv ATP was also tested on water intake induced by intragastric load of 12% NaCl (2 mL/rat), acute treatment with the diuretic/natriuretic furosemide (20 mg/kg), icv angiotensin II (50 ng/µL) or icv carbachol (a cholinergic agonist, 4 nmol/µL), on sodium depletion-induced 1.8% NaCl intake, and on food intake induced by food deprivation. Male Holtzman rats (280-320 g, N = 7-11) had cannulas implanted into the lateral ventricle. Icv ATP (300 nmol/µL) reduced water intake induced by water deprivation (13.1 ± 1.9 vs saline: 19.0 ± 1.4 mL/2 h; P < 0.05), an effect blocked by pre-treatment with PPADS, but not DPCPX. Icv ATP also reduced water intake induced by NaCl intragastric load (5.6 ± 0.9 vs saline: 10.3 ± 1.4 mL/2 h; P < 0.05), acute furosemide treatment (0.5 ± 0.2 vs saline: 2.3 ± 0.6 mL/15 min; P < 0.05), and icv angiotensin II (2.2 ± 0.8 vs saline: 10.4 ± 2.0 mL/2 h; P < 0.05), without changing icv carbachol-induced water intake, sodium depletion-induced 1.8% NaCl intake and food deprivation-induced food intake. These data suggest that central ATP, acting on purinergic P2 receptors, reduces water intake induced by intracellular and extracellular dehydration.

Adenosine deaminase activity as a biochemical marker of inflammatory response in goats infected by caprine arthritis-encephalitis virus

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Negative chronotropic response to adenosine receptor stimulation in rat right atria after run training

The aim of the present study was to evaluate the potency and maximal responses (E-max) to the adenosine receptor agonists N-6-cyclopentyladenosine (CPA), N-ethylcarboxamidoadenosine (NECA) and N-6-(3-iodobenzyl)-5'-N-methylcarbaxamidoadenosine (IB-MECA) in right atria from trained rats. We also investigated the interaction between the training bradycardia and the sensitivity of the chronotropic response mediated by adenosine receptor stimulation.2. Animals were submitted to run training for 60 min, 5 days a week, over a period of 8 weeks. Mean blood pressure and heart rate were measured in conscious animals. Right atria were isolated and concentration-response curves to CPA, NECA and IB-MECA were obtained.3. A reduction in heart rate was found in trained rats, indicating that the training programme was successful in inducing physical conditioning. The three adenosine receptor agonists induced a concentration-dependent negative chronotropic response. The rank order of potency and E-max for the three adenosine receptor agonists was CPA>NECA>IB-MECA.4. Dynamic exercise for 8 weeks did not alter the E a, for CPA, NECA and IB-MECA. Similarly, the potencies of CPA and NECA were not affected by run training, whereas the potency of IB-MECA was reduced (6.10+/-0.09 vs 5.66+/-0.10 for sedentary and trained groups, respectively).5. In conclusion, run training for 8 weeks induced a desensitization of the chronotropic response to IB-MECA without changing the potency of CPA and NECA. These findings exclude the participation of adenosine receptors in the training bradycardia.

The potentiation of the histamine release induced by adenosine in mast cells from guinea pig lung and heart: Sharp dependence on the time of preincubation

We studied here the effect of a wide range of adenosine concentration and time of preincubation, on the histamine release induced in the guinea pig mast cells by different stimulus. Adenosine (10(-5)-10(-3) M) potentiated the histamine release induced by antigen in the guinea pig heart (isolated and dispersed tissue) and lung mast cells but not induced by ionophore A23197. The potentiation caused by adenosine (10(-4) M) was maximum after 1-3 min of preincubation and is probably an extracellular effect since it was not avoided by dipyridamol (3 x 10(-7)-10(-6) M) that inhibit the uptake of adenosine. Similar potentiation was also produced by the adenosine mimetic 2-chloroadenosine (10(-5) M) and both effects were inhibited by 8-phenyltheophylline indicating an effect on the type A receptors. It is suggested that the adenosine potentiation may not be related to changes on the cyclic AMP levels. (C) 2000 Academic Press.

The effect of ions and adenosine nucleotides on the activity of lactate dehydrogenase from the epaxial muscle of fish

Lactate dehydrogenase was partially purified from the epaxial muscle of Piaractus mesopotamicus (pacu) and its hybrid Piaractus mesopotamicus x Colossoma macropomus (tambacu). This preparation was used for kinetic studies carried out at pH 6.0 and 7.5. It was also used for the study of the inhibition properties of adenosine nucleotides = ATP, ADP, AMP =, divalent ions Ni2+, Cu2+, Co2+ and the anions oxamate and oxalate.

Type-2 diabetes mellitus and the frequency of the G22A polymorphism of the adenosine deaminase gene in a mixed population in Brazil

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Amplification of neuromuscular transmission by methylprednisolone involves activation of presynaptic facilitatory adenosine A(2A) receptors and redistribution of synaptic vesicles

The mechanisms underlying improvement of neuromuscular transmission deficits by glucocorticoids are still a matter of debate despite these compounds have been used for decades in the treatment of autoimmune myasthenic syndromes. Besides their immunosuppressive action, corticosteroids may directly facilitate transmitter release during high-frequency motor nerve activity. This effect coincides with the predominant adenosine A(2A) receptor tonus, which coordinates the interplay with other receptors (e.g. muscarinic) on motor nerve endings to sustain acetylcholine (ACh) release that is required to overcome tetanic neuromuscular depression in myasthenics. Using myographic recordings, measurements of evoked [H-3]ACh release and real-time video microscopy with the FM4-64 fluorescent dye, results show that tonic activation of facilitatory A(2A) receptors by endogenous adenosine accumulated during 50 Hz bursts delivered to the rat phrenic nerve is essential for methylprednisolone (03 mM)-induced transmitter release facilitation, because its effect was prevented by the A(2A) receptor antagonist, ZM 241385 (10 nM). Concurrent activation of the positive feedback loop operated by pirenzepine-sensitive muscarinic M-1 autoreceptors may also play a role, whereas the corticosteroid action is restrained by the activation of co-expressed inhibitory M-2 and Al receptors blocked by methoctramine (0.1 mu M) and DPCPX (2.5 nM), respectively. Inhibition of FM4-64 loading (endocytosis) by methylprednisolone following a brief tetanic stimulus (50 Hz for 5 s) suggests that it may negatively modulate synaptic vesicle turnover, thus increasing the release probability of newly recycled vesicles. Interestingly, bulk endocytosis was rehabilitated when methylprednisolone was co-applied with ZM241385. Data suggest that amplification of neuromuscular transmission by methylprednisolone may involve activation of presynaptic facilitatory adenosine A(2A) receptors by endogenous adenosine leading to synaptic vesicle redistribution. (C) 2014 Elsevier Ltd. All rights reserved.