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At least 901 records · Page 50Linked to original sources
PubMed2001

Differential regulations between adenosine triphosphate (ATP)- and uridine triphosphate-induced Cl(-) secretion in bovine tracheal epithelium. Direct stimulation of P1-like receptor by ATP.

Adenosine 5'-triphosphate (ATP) stimulates airway epithelial Cl(-) secretion in a complicated manner. We examined the difference between ATP- and uridine 5'-triphosphate (UTP)-induced responses of short-circuit current (Isc) in bovine tracheal epithelium treated with amiloride. Each nucleotide caused an increase in Isc composed of the first and second peaks, where the second peak induced by ATP was higher compared with UTP. The ATP-induced second peak was inhibited by the protein kinase (PK) A inhibitor H89, saturation of P1 receptor with adenosine, and the P1 receptor antagonist 8-p-sulfophenyltheophylline, but not by the Ca(2+) chelator ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid plus the endoplasmic reticulum Ca(2+)-pump inhibitor thapsigargin, the adenosine breakdown enzyme adenosine deaminase, the ectonucleotidase inhibitor alpha,beta-methyleneadenosine 5'-diphosphate, or saturation of P2Y2 receptor with UTP. Thus, the response is associated with PKA-dependent pathway via P1-like receptor but not with Ca(2+)-dependent pathway via P2Y2 receptor, and ATP degradation products do not contribute to this response. Further, stimulation of cells with ATP increased PKA activity. In addition, pretreatment with glybenclamide, an inhibitor of cystic fibrosis transmembrane conductance regulator, reduced the second peak of Isc induced by ATP but was without effect on that induced by UTP. Therefore, ATP stimulates glybenclamide-sensitive Cl(-) secretion, and this action is partly mediated by PKA-dependent pathway via P1-like receptor.

Adenosine↗
PubMed2004

A mitochondrial ATPase 6 mutation is associated with Leigh syndrome in a family and affects proton flow and adenosine triphosphate output when modeled in Escherichia coli.

A multidisciplinary strategy was used to identify the molecular defect in a family with Leigh syndrome (LS). The propositus presented severe developmental delay, an ataxic-spastic gait and seizures. She died at 3.5 y of age from cardiorespiratory arrest. Postmortem examination disclosed pathological features typical of LS. A 12-y-old sister is affected with the same disease. Respiratory chain enzyme complex activities in skeletal muscle biopsy were normal. Adenosine triphosphate (ATP) synthesis during oxidative phosphorylation in skin fibroblasts mitochondria showed a severely hampered ATP production. Mitochondrial DNA sequencing revealed a new mutation in the ATPase 6 gene (T9176G). Site-directed mutagenesis in Escherichia coli strains was used to measure H+ pumping and ATP synthesis. Results were comparable to findings obtained in human cells. These data corroborate the use of E. coli strains as a feasible "animal" model for functional studies in pathogenic mutations of the ATPase 6 gene.

Child↗
PubMed2004

Prognostic value of stress myocardial perfusion imaging using adenosine triphosphate at the beginning of haemodialysis treatment in patients with end-stage renal disease.

BACKGROUND: Non-invasive detection of coronary artery disease (CAD) remains difficult in patients with end-stage renal disease (ESRD). This study evaluated the ability of pharmacologic stress myocardial perfusion imaging to predict cardiac events in patients with ESRD. METHODS: A prospective study was carried out in 49 consecutive patients with ESRD. Thallium-201 single photon emission computed tomography (SPECT) using high-dose adenosine triphosphate (ATP) was performed within 1 month of the beginning of haemodialysis. The study end-point was a cardiac event or the 1-year anniversary of the SPECT study. RESULTS: Twenty-four patients (17 diabetics, 57% and seven non-diabetics, 37%) had myocardial perfusion defects. The remaining 25 patients had normal perfusion images. Fifteen patients had non-fatal cardiac events and two patients died of a cardiac cause. All patients who had non-fatal cardiac events underwent myocardial revascularization and survived until the end of follow-up. The 1-year cardiac event-free survival rate was 34% among patients with perfusion defects and 96% among patients without perfusion defects (P<0.001). The presence of a myocardial perfusion defect was the only independent predictor of 1-year cardiac events both in overall (HR, 49.91; 95% CI, 5.15-484.00; P<0.001) and in diabetic patients (HR, 33.72; 95% CI, 2.96-383.5; P = 0.005). Diabetes and an increased C-reactive protein were associated with the progression of CAD. CONCLUSIONS: Normal myocardial perfusion imaging by stress thallium-201 SPECT using high-dose ATP performed within 1 month after the beginning of haemodialysis treatment is a powerful predictor of cardiac event-free survival in patients with ESRD.

Cardiovascular Diseases↗
PubMed2006

Cosignaling of adenosine and adenosine triphosphate in hypobaric hypoxia-induced hypothermia.

Purines, that is, adenosine and ATP, are not only products of metabolism but are also neurotransmitters. Indeed, purinergic neurotransmission is involved in thermoregulatory processes that occur during normoxia. Exposure to severe hypoxia elicits a sharp decrease in body core temperature (T(CO)), and adenosinergic mechanisms have been suspected to be responsible for this hypothermia. Because ATP per se and its metabolite adenosine could have complex interactions in some neural networks, we hypothesize that both adenosine and ATP are involved in the central mechanism of hypoxia-induced hypothermia. Their role in the thermoregulatory process was therefore investigated in a 24-h hypobaric hypoxia (Fi(O2) = 10%), using CGS-15943, a nonselective antagonist of adenosine receptors, and suramin, an ATP receptor antagonist. T(CO) and spontaneous activity (A(S)) were monitored by telemetry in conscious rats, receiving CGS-15943 (10 mg/kg ip), suramin (7 nmol icv), or both. The same treatments were done in normoxia to evaluate the specificity of their thermoregulatory action observed in hypoxia. Suramin/CGS-15943 treatment blunted the profound hypothermia observed in control rats throughout the hypoxia exposure, whereas CGS-15943 treatment blunted hypothermia during only 3 h, and suramin treatment had no effect. These results suggest that suramin potentiates the CGS-15943 effects and consequently that adenosine and ATP signaling act in synergy. In normoxia, suramin/CGS-15943 induced an increase in T(CO) but to a far lesser extent than observed in hypoxia. Thus it might be suggested that the suramin/CGS-15943 blunting of hypoxia-induced hypothermia would be specific to hypoxia-induced mechanisms.

Adenosine↗
PubMed1994

Accumulation of the adenosine triphosphate synthase subunit C in the mnd mutant mouse. A model for neuronal ceroid lipofuscinosis.

The motor neuron degeneration (mnd) mutant mouse, initially described as an autosomal semidominant model of motor neuron disease, is characterized by progressive loss of motor activities and the accumulation of lipofuscin-like material in the cytoplasm of neurons in many regions of the nervous system. The stored material is composed of granular, multilamellar, fingerprint, and curvilinear profiles and degenerating mitochondria. These inclusions are associated with the accumulation of subunit c of mitochondrial adenosine triphosphate synthase in an age-dependent pattern. These abnormalities first appear in neurons of the thalamus, hippocampus, and cortex and eventually involve virtually all nerve cells, including those in the retina and enteric nervous system. This type of neuropathology and the presence of subunit c in neurons of mnd mutant mice are characteristic features of neuronal ceroid lipofuscinosis (NCL). The murine disease resembles Batten's disease, an autosomal recessive disorder and the most common NCL in humans. The mnd mouse should be of great value for investigations of the genetics of NCL, for studies designed to delineate the mechanism that lead to neuronal degeneration in these disorders, and for testing novel therapeutic approaches.

Animals↗