Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.25 (triphosphatase)
 1,529 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The teleostean gill is characterized by an exceptionally low permeability to water. Water moves along the osmotic gradient across the gill, being gained in fresh water and lost in sea water. Coupling of water movement to solute movement has not been reported. In fresh water, the gill is the site of independent active uptake of sodium and chloride. Na+ uptake is coupled to H+ or NH4+ excretion, Cl- uptake to HCO3- excretion. Amiloride blocks sodium transport and thiocyanate inhibits the chloride pump. In sea water, sodium and chloride exchanges across the gill are about 100 times faster than in fresh water, up to 100% of the internal sodium or chloride being exchanged per hour. Chloride is actively excreted, while sodium movement may well be passive. The chloride pump is associated with a mechanism for Na/K exchange; both pump and Na/K exchange are blocked by thiocyanate and possibly by ouabain. Three enzymes are involved in the ionic pumps: carbonate dehydratase (EC 4.2.1.1; carbonic anhydrase), sodium/potassium-stimulated adenosine-triphosphatase (EC 3.6.1.3, ATPase) and anion-stimulated ATPase. Specialized cells ('chloride cells') are presumably the site of the active transport.
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PMID:Transport of ions and water across the epithelium of fish gills. 0 38

The effect of isoproterenol on the electrophysiological properties of the S2 proximal segment of the rabbit was examined. Isoproterenol at 10(-8) to 10(-4) M depolarized the basolateral membrane voltage (Vb) in a dose-dependent manner. Propranolol attenuated the isoproterenol-induced depolarization. These possible mechanisms of cell depolarization were explored. The role of luminal Na(+)-organic solute cotransport was negligible, since the removal of organic solute did not change the depolarization. Basolateral Na(+)-(HCO3-) cotransport was supported by the finding that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited isoproterenol-induced depolarization. Basolateral K+ conductance was suggested by the finding that the application of Ba2+ blocked the isoproterenol-induced depolarization. Na(+)-K(+)-adenosine-triphosphatase (ATPase) was questionable. Although ouabain blocked isoproterenol-induced depolarization, the removal of Na+ did not inhibit the depolarization. Further experiment revealed that dibutylyl-adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromo cAMP, and forskolin did not mimic the response of isoproterenol. These results demonstrate: 1) there is a functional beta-adrenoceptor that depolarizes Vb; 2) isoproterenol-induced depolarization is due to an inhibition of basolateral K+ channel or the activation of basolateral Na(+)-(HCO3-)n cotransport; 3) isoproteronol-induced depolarization is independent of cAMP in the rabbit proximal tubule.
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PMID:Evidence for presence of functional beta-adrenoceptor in rabbit S2 proximal straight tubules. 165 31