PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
1336929-6	1992	Amiloride (1 mM) acidified pHi but DIDS (1 mM) treatment, HCO3(-)-free condition, 1 mM ouabain, 50 mM K+, and 2 mM BaCl2 failed to change pHi.	Amiloride	0-9	glucose-6-phosphate isomerase	Bos taurus	27-30	
10886036-5	2000	For cells at steady-state pHi, resuspension in hyperosmotic solutions elicited an alkalinization, which was significantly inhibited by removal of extracellular Na+ ions, or treatment with amiloride (1 mM) or HOE-694 (10 microM), both inhibitors of Na+ x H+ exchange.	Amiloride	188-197	glucose-6-phosphate isomerase	Bos taurus	26-29	
19050954-7	2009	pHi recovery was also greatly reduced in the presence of 4,4"-diisothiocyanatostilbene-2,2"-disulfonic acid (DIDS) and amiloride.	Amiloride	119-128	glucose-6-phosphate isomerase	Bos taurus	0-3	
1335884-4	1992	Cell acidifications (pHi to 6.65, n = 8) induced by the "NH(4+)-loading" method were rapidly followed by a Na(+)-dependent, amiloride-inhibitable pHi recovery.	Amiloride	124-133	glucose-6-phosphate isomerase	Bos taurus	21-24	
1335884-4	1992	Cell acidifications (pHi to 6.65, n = 8) induced by the "NH(4+)-loading" method were rapidly followed by a Na(+)-dependent, amiloride-inhibitable pHi recovery.	Amiloride	124-133	glucose-6-phosphate isomerase	Bos taurus	146-149	
1335884-8	1992	Consistent with this posit, the reintroduction of Na+ to cells perfused in the absence of the cation with a HCO3(-)-containing, amiloride-complemented solution resulted in a gradual recovery from the acidic pHi induced by the baseline conditions (n = 6).	Amiloride	128-137	glucose-6-phosphate isomerase	Bos taurus	207-210	
2832823-3	1988	(1) Regulation of pHi after induction of an acid load by removal of NH4Cl could be blocked either totally by removal of extracellular sodium, or subtotally (about 90%) by application of amiloride (1 mmol/l).	Amiloride	186-195	glucose-6-phosphate isomerase	Bos taurus	18-21	
1328110-6	1992	Steady-state pHi was reduced by addition of 0.5 mmol/l amiloride, a Na+/H+ exchange blocker (-.16 pH U for FBCE, -.18 for CBCE) or removal of Na+ (-.47 pH U for FBCE, -.51 for CBCE).	Amiloride	55-64	glucose-6-phosphate isomerase	Bos taurus	13-16	
1919580-4	1991	The pHi returned toward the basal pH value after acidification within 5-10 min in the presence of Na+ or Li+, but the pHi stayed acidic when Na(+)-free buffers were used or in the presence of amiloride and its analogues.	Amiloride	192-201	glucose-6-phosphate isomerase	Bos taurus	118-121	
2848042-5	1988	In the presence of 1 mM amiloride or in the absence of Na+, this process was blocked, indicating the involvement of an Na+/H+ exchanger in the regulation of pHi after an acid load.	Amiloride	24-33	glucose-6-phosphate isomerase	Bos taurus	157-160	
1335564-5	1992	Amiloride (1 mM) caused an acidification of approximately 0.2 U within 2 min: replacement with normal Ringer allowed a return to normal pHi after an alkali overshoot.	Amiloride	0-9	glucose-6-phosphate isomerase	Bos taurus	136-139	
3184169-3	1988	Following an acid load imposed by a NH4Cl prepulse, pHi was regulated in the absence of HCO3- by a Na+-dependent process inhibitable to a large extent by 1 mM amiloride and 0.1 mM dimethylamiloride.	Amiloride	159-168	glucose-6-phosphate isomerase	Bos taurus	52-55	
2841075-9	1988	Application of 1 mM amiloride reversibly inhibited pHi recovery.	Amiloride	20-29	glucose-6-phosphate isomerase	Bos taurus	51-54