Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between the oxygen uptake and the release of amylase and sialic acid induced by pilocarpine was investigated in dog submandibular glands. Pilocarpine dose-dependently stimulated the oxygen uptake. The dose required for the maximal response was 10 microM. The release of amylase and sialic acid induced by pilocarpine was inhibited by the addition of iodoacetic acid, malonic acid, 2, 4-dinitrophenol, antimycin A or sodium azide. The oxygen uptake induced by pilocarpine was significantly inhibited by iodoacetic acid, malonic acid, antimycin A or sodium azide. On the other hand, 2, 4-dinitrophenol further stimulated the oxygen uptake by pilocarpine. The increase in the oxygen uptake or the release of amylase and sialic acid induced by pilocarpine was significantly inhibited by ouabain. The Na+, K+-ATPase activity ratio in the microsomal fraction of dog submandibular glands was dose-dependently increased by pilocarpine. The Na+, K+-ATPase activity ratio induced by pilocarpine was significantly inhibited by ouabain, antimycin A, oligomycin or 2, 4-dinitrophenol. The pilocarpine-induced Na+, K+-ATPase activity ratio was significantly inhibited by the removal Ca2+ from the medium or the addition of 2 mM EGTA. These results suggest that the increase in the oxygen uptake by pilocarpine is profoundly involved in the energy supply for the process of amylase and sialic acid release. In particular, the energy supply demanded for the activation of Na+ pump may play a role in the mechanism by which pilocarpine induces the oxygen uptake.
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PMID:[Studies on the relationship between the oxygen uptake and the release of amylase and sialic acid]. 241

Male Sprague-Dawley rats received 4 mg pilocarpine/100 g body wt intraperitoneally or physiological saline as control and were killed at various intervals. Acid phosphatase was reacted on frozen sections from soft palate, parotid and submandibular glands using sodium-alpha-naphthyl acid phosphate as substrate. Various inhibitors were added to the incubation medium. The strongest acid phosphatase activity was in the parotid gland acinar and proximal secretory duct cells; the mucous minor glands of the palate were completely negative. Activity was found in the acinar cells, proximal secretory duct cells, granular and striated duct and excretory duct cells. Pilocarpine injection slightly reduced the activity up to 6 h after injection. Cupric chloride added to the incubation medium lowered the overall activity. Fluoride and molybdate inhibited the acid phosphatase reaction in all structures. Tartrate inhibited the reaction in all structures except the submandibular striated duct cells. The tartrate-resistant activity may be a Na+K+-dependent ATPase involved in re-absorbing water and electrolytes from the primary saliva.
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PMID:A histochemical study of rat salivary gland acid phosphatase. 346 May 42

Pilocarpine is an alkaloid obtained from the leaves of Pilocarpus genus, with important pharmaceutical applications. Previous reports have investigated the production of pilocarpine by Pilocarpus microphyllus cell cultures and tried to establish the alkaloid biosynthetic route. However, the site of pilocarpine accumulation inside of the cell and its exchange to the medium culture is still unknown. Therefore, the aim of this study was to determine the intracellular accumulation of pilocarpine and characterise its transport across membranes in cell suspension cultures of P. microphyllus. Histochemical analysis and toxicity assays indicated that pilocarpine is most likely stored in the vacuoles probably to avoid cell toxicity. Assays with exogenous pilocarpine supplementation to the culture medium showed that the alkaloid is promptly uptaken but it is rapidly metabolised. Treatment with specific ABC protein transporter inhibitors and substances that disturb the activity of secondary active transporters suppressed pilocarpine uptake and release suggesting that both proteins may participate in the traffic of pilocarpine to inside and outside of the cells. As bafilomicin A1, a specific V-type ATPase inhibitor, had little effect and NH4Cl (induces membrane proton gradient dissipation) had moderate effect, while cyclosporin A and nifedipine (ABC proteins inhibitors) strongly inhibited the transport of pilocarpine, it is believed that ABC proteins play a major role in the alkaloid transport across membranes but it is not the exclusive one. Kinetic studies supported these results.
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PMID:Characterisation of the membrane transport of pilocarpine in cell suspension cultures of Pilocarpus microphyllus. 2547 86