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Start Over Descriptor "Amiloride" Publisher springer-verlag
241 results on '"Amiloride"'

1. The effect of acetazolamide, amiloride, bumetanide and SITS on secretion of fluid and electrolytes by the parotid gland of common wombats, Vombatus ursinus.

Author

Beal AM

Subjects
Acetazolamide pharmacology, Animals, Bicarbonates, Chlorides, Electrolytes, Parotid Gland, Salivary Glands, Amiloride, Bumetanide pharmacology
Abstract

Mechanisms of saliva formation by wombat parotid glands were investigated in anaesthetized wombats at two levels of cholinergically-stimulated flow viz. mid-range (30-40% maximum flow) and maximum flow using ion-transport and carbonic-anhydrase inhibitors. Bumetanide (0.005-0.1 mmol l -1 carotid plasma) progressively reduced mid-range flow by 52 ± 3.4% (mean ± SEM). Concurrently, saliva [Cl] decreased, [Na] and [HCO 3 ] increased but HCO 3 excretion was unaltered. Salivary flow during high-rate cholinergic stimulation was 31 ± 1.1% of the pre-bumetanide maximum. During mid-range stimulation, SITS (0.075 mmol l -1 ) was without effect whereas 0.75 mmol l -1 stimulated transient increases in fluid output. The higher SITS concentration caused no alterations to flow or electrolyte concentrations during maximal stimulation. Carotid plasma [amiloride] (0.05 mmol l -1 ) caused immediate falls in flow rate of 20-30% followed by progressive recovery over 25 min to levels above pre-amiloride flow rates despite plasma [amiloride] increasing tenfold. Concurrently, salivary [Na] and [Cl] rose to equal plasma concentrations and [K] fell by 50% indicating blockade of acinar Na/H exchangers and luminal Na channels in the ducts. Increased salivary osmolarity caused the flow recovery. Saliva flow during maximum cholinergic stimulation was reduced by 38-46%. The depression of flow was interpreted as resulting from competition between amiloride and acetylcholine for access to the muscarinic receptors. Plasma [acetazolamide] (0.35-2.5 mmol l -1 ) did not alter saliva outflow during mid-range or maximum flow regimes whereas salivary [Cl] increased and [HCO 3 ] decreased consistent with reduced anion exchange resulting from inhibition of carbonic anhydrase. Combined with bumetanide, acetazolamide (1.5 mmol l -1 ) reduced flow by an additional 18-22% relative to bumetanide alone thereby demonstrating that acinar HCO 3 synthesis supported a limited proportion of saliva formation and that some HCO 3 secretion was independent of carbonic anhydrase activity.

Published
2021
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2. Cleavage of endogenous γENaC and elevated abundance of αENaC are associated with increased Na+ transport in response to apical fluid volume expansion in human H441 airway epithelial cells

Author

Indusha A. Selvanathar, Deborah L. Baines, and Chong D. Tan

Subjects
Epithelial sodium channel, Physiology, Clinical Biochemistry, ENaC, Respiratory Mucosa, Na+ transport, Cell Line, Amiloride, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Cell polarity, Extracellular, medicine, Animals, Humans, Protease Inhibitors, Epithelial Sodium Channels, Furin, 030304 developmental biology, Cell Size, 0303 health sciences, Ussing chamber, biology, Sodium, Cell Polarity, Epithelial Cells, Apical membrane, Proprotein convertase, Cell biology, Protease, Electrophysiology, Airway, biology.protein, 030217 neurology & neurosurgery, Ion Channels, Receptors and Transporters, medicine.drug, Sodium Channel Blockers
Abstract

Using human H441 airway epithelial cells cultured at air–liquid interface (ALI), we have uniquely correlated the functional response to apical fluid volume expansion with the abundance and cleavage of endogenous α- and γENaC proteins in the apical membrane. Monolayers cultured at ALI rapidly elevated Isc when inserted into fluid-filled Ussing chambers. The increase in Isc was not significantly augmented by the apical addition of trypsin, and elevation was abolished by the protease inhibitor aprotinin and an inhibitor of the proprotein convertase, furin. These treatments also increased the IC50 amiloride indicating that the effect was via inhibition of highly Na+-selective ENaC channels. Apical fluid, 5–500 μl for 1 h in culture, increased the spontaneous starting Isc in a dose-dependent manner, whilst maximal fluid-induced Isc in the Ussing chamber was unchanged. Apical fluid expansion increased the abundance of 63–65-kDa αENaC proteins in the apical membrane. However, this could not be attributed to increased cleavage as protease inhibitors had no effect on the ratio of cleaved to non-cleaved (90 kDa) αENaC proteins. Instead, fluid expansion increased αENaC abundance in the membrane. In contrast, function correlated well with γENaC cleavage at known sites by furin and extracellular proteases. Interestingly, cleavage of γENaC was associated with increased retrieval from the membrane via the proteosomal pathway. Thus, the response to apical fluid volume expansion in H441 airway epithelial cells involves cleavage of γENaC, and changes in α- and γENaC protein abundance at the apical membrane. Electronic supplementary material The online version of this article (doi:10.1007/s00424-011-0982-x) contains supplementary material, which is available to authorized users.

Published
2011

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