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At least 1,297 records · Page 72Linked to original sources
PubMed1997

Adenosine triphosphate attenuates renal sympathetic nerve activity through left ventricular chemosensitive receptors.

We previously reported that ATP, but not adenosine, administered i.v. attenuates the baroreflex-mediated increase in sympathetic nerve activity in response to arterial hypotension by a vagal afferent mechanism. It was not elucidated in that study which vagal afferent endings are involved. Mongrel dogs were anesthetized with alpha-chloralose, thoracotomy was performed and a 27-gauge hypodermic needle was inserted into the left circumflex coronary artery. The left renal sympathetic nerves were isolated and placed on a bipolar silver electrode for measurement of renal sympathetic nerve activity (RSNA). Dose-response effects of intracoronary or i.v. infusion of ATP (100, 200 or 400 microg/kg/min) on RSNA and mean arterial pressure were studied in neuraxis-intact and cervically vagotomized dogs. RSNA was increased dose-dependently with decreasing mean arterial pressure during the i.v. ATP infusion. Elevation of RSNA was attenuated by higher intracoronary ATP infusion rates, despite the fact that mean arterial pressure was decreased dose-dependently. Left ventricular end-diastolic pressure, however, remained unchanged. This suppression of RSNA by the intracoronary ATP infusion was completely abolished by bilateral cervical vagotomy. Our data suggest that ATP attenuates reflex increases in sympathetic nerve activity by possibly stimulating ventricular chemoreceptors with cardiac vagal afferents.

Adenosine Triphosphate↗
PubMed2000

Neurotransmitters adenosine triphosphate and noradrenaline induce nitric oxide release in rat vas deferens.

1. In rat vas deferens, electrical field stimulation (EFS) evoked a muscular biphasic tetrodotoxin (TTX)-sensitive contractile response. 2. The amplitude of this response increased with the frequency of stimulation. 3. After each stimulation, nitric oxide (NO) release was assayed and found to be released in a frequency-dependent manner. 4. NO release also occurred after treatment with exogenous neurotransmitters, adenosine 5'-triphosphate (ATP) and noradrenaline (NA). 5. Prazosin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), respective antagonists of alpha1-adrenoceptors and P2x purinoceptors, inhibited NO release induced by NA and ATP. Both prazosin and PPADS inhibited NO release by EFS. 6. TTX failed to modify the NO release induced by exogenous neurotransmitters but abolished the release of NO and contractile response by EFS. 7. EFS and released noradrenaline and ATP induce the release of NO through postjunctional alpha1 -adrenoceptors and P2x-purinoceptors, respectively.

Adenosine Triphosphate↗
PubMed1992

Degranulation of rough endoplasmic reticulum in M phase and adenosine-triphosphate-treated interphase cells is reversible.

In the preferential harvesting of rounded mitotic (M phase) cells of human Chang liver monolayer cultures by mechanical agitation in Ca(2+)-free phosphate-buffered saline, degranulation of endoplasmic reticulum (ER) was observed. Mitotic cells are known to have a series of Ca2+ transients and, without being subjected to Ca(2+)-free washings, did not have degranulated ER. Quiescent cells incubated with 0.7 mM adenosine 5'-triphosphate (ATP) in Ca(2+)-free HEPES-buffered saline produced very similar ER degranulations. Confocal argon laser imaging of fluo-3-loaded cells showed a Ca2+ transient peaking at 2 min after ATP treatment. In the absence of extracellular Ca2+, transients of Ca2+ elevation in the cytosol would exit the cell in a down-gradient, draining the ER Ca2+ stores. Substituting ATP with 1 microM brominated A23187 calcium ionophore in the incubation that contained 1-100 mM CaCl2, respectively, did not produce ER degranulation, thereby excluding raised cytosolic Ca2+ per se as the cause of ER degranulation. In fact, incubation with 0.7 mM ATP in the presence of 1-5 mM CaCl2 failed to produce ER degranulation. ER degranulated cells, from treatment with ATP without extracellular Ca2+ as well as from Ca(2+)-free washings at M phase, could be rescued by subsequent incubation in growth medium that contains Ca2+ whereupon the rounded cells re-flatten (a round-to-flat change) and have well-defined rough ER. It therefore seems possible for Ca2+ depletion, or at least a reduction, to be causally related to ER degranulation. If that were the case, ER granularity would appear to be a facultative rather than a constitutive state.

Adenosine Triphosphate↗