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At least 883 records · Page 49Linked to original sources
PubMed1975

The effects of halothane and enflurane on rat brain synaptosomal sodium-potassium-activated adenosine triphosphatase.

Synaptosomes, or nerve-ending particles, were isolated from the cerebral cortices of young rats by homogenization, differential centrifugation, and density-gradient centrifugation. The sodium-potassium-activated adenosine triphosphatase enzyme system [(Na+ plus K+)-ATPase] of these particles is believed to represent in vitro the sodium-potassium pump of the nerve terminal. Suspensions of synpatosomes were equilibrated with air containing various concentrations of halothane and enflurane, as determined by gas chromatography. Clinical concentrations of the anesthetics had no effect on (Na+ plus K+)-ATPase activity. Fourteen per cent halothane and 14.8 per cent enflurane in the gas phase resulted in 12 and 10 per cent inhibition, respectively, of (Na+ plus K+)-ATPase activity. These data confirm that interference with active cation transport by inhibition of neuronal (Na+ plus K+)-ATPase is not related to the mechanism of halothane or enflurane anesthesia. (Key words: Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Metabolism, enzymes, ATPase; Nerve, synaptosomal ATPase; Theories of anesthesia, ATPase.).

Adenosine Triphosphate↗
PubMed1980

Primary structure of the calcium ion-transporting adenosine triphosphatase from rabbit skeletal sarcoplasmic reticulum. Some peptic, thermolytic, tryptic and staphylococcal-proteinase peptides.

The soluble peptides from the peptic digest of the reduced S-carboxymethylated 3-carboxypropionylated adenosine triphosphatase protein have been isolated and most of their structures have been determined. About 397 residues of the protein were represented in these peptides. The reduced S-carboxymethylated protein was digested with thermolysin, and peptides containing arginine or carboxymethylcysteine were isolated and characterized. Some peptides isolated from tryptic and staphylococcal-proteinase digests of the protein are described. The information contained within the structures of these peptides has been used to reconstruct long stretches of the sequence of the ATPase protein that constitute most of the protein structure external to the lipid bilayer (Allen, Trinnaman and Green (1980) Biochem. J. 187, 591-616). The details of some of the chromatographic steps used in the isolation of the peptides and the properties of the peptides are contained in Supplementary Publication SUP 50104 (45 pages), which has been deposited with the British Library Lending Division, Boston Spa, Wetherby, West Yorkshire LS23 7BQ, U.K., from whom copies can be obtained on the terms indicated in Biochem. J. (1978) 169, 5.

Amino Acid Sequence↗
PubMed2001

Relation of alleles of the sodium-potassium adenosine triphosphatase alpha 2 gene with blood pressure and lead exposure.

Lead is associated with elevated blood pressure, although the mechanism of action is unknown. Genetic differences in sodium-potassium adenosine triphosphatase (Na(+)-K(+)ATPase) could explain some of the variation in the strength of the blood pressure-blood lead relation that has been observed in previous studies. In 1996-1997, the authors studied the association of blood pressure, hypertension prevalence, and polymorphisms in the gene for the alpha 2 subunit of Na(+)-K(+)ATPase (ATP1A2) among 220 former organolead manufacturing workers from New Jersey. Subjects were genotyped for a restriction fragment length polymorphism (RFLP) on the ATP1A2 gene. The association between blood lead and blood pressure was stronger among persons who were homozygous for the variant allele. Genotype was also associated with hypertension (adjusted odds ratio = 7.7; 95% confidence interval: 1.9, 31.4). Finally, the variant allele was 1.8 times more common among African Americans than among Caucasians. The RFLP may indicate susceptibility to the effect of lead on blood pressure. Moreover, the alpha 2 gene (or a closely linked gene) may contribute to the pathophysiology of hypertension. However, because the number of subjects (especially African Americans) with the susceptible genotype in this study was small, these observations should be considered preliminary.

Adult↗
PubMed1995

Effects of ranitidine on gastric vesicles containing H+,K(+)-adenosine triphosphatase in rats.

BACKGROUND: To ascertain the mechanism for rebound acid hypersecretion after treatment with an H2-receptor blocker, we investigated the effects of ranitidine on gastric H+,K(+)-adenosine triphosphatase (ATPase) in rats. METHODS: Male Wistar rats received ranitidine (1-50 mg/kg body weight intraperitoneally twice a day for 5 days). The rats were starved for 15 h after the last treatment and then killed, and gastric vesicles containing H+,K(+)-ATPase were prepared. RESULTS: Treatment with ranitidine dose-dependently increased protein content in the gastric vesicular fraction purified from the gastric mucosa without changing total protein content. Ranitidine also increased the content of a 94,000-dalton protein, the catalytic subunit of H+,K(+)-ATPase. On the other hand, ranitidine did not affect the specific activity of the enzyme (mumol/min/mg of the gastric vesicular protein). Since gastric vesicles in the fasting state mainly consist of the tubulovesicular membrane, these results suggest that ranidine administration increases total tubulovesicular H+,K(+)-ATPase content (mumol/min/rat) by increasing the number of tubulovesicles per parietal cell. The ranitidine-induced increase in total tubulovesicular H+,K(+)-ATPase activity was still evident 1 week after treatment and returned to control level 1 month later. CONCLUSIONS: All these findings suggest that the increased content and total activity of tubulovesicular H+,K(+)-ATPase after ranitidine treatment may contribute to the mechanism for acid rebound after H2-blocker therapy.

Animals↗