PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15539434-6	2005	ACh induced a prominent acidification of pH(i) in the presence of HCO(3)(-), and the acidification was further increased by EIPA treatment.	Bicarbonates	66-72	acyl-CoA thioesterase 12	Rattus norvegicus	0-3	
15539434-3	2005	In the HCO(3)(-)-free condition, the V(h,ACh) was also blocked by bumetanide, a blocker of Na(+)-K(+)-2Cl(-) cotransporter (NKCC).	Bicarbonates	7-16	acyl-CoA thioesterase 12	Rattus norvegicus	41-44	
15539434-4	2005	In the presence of HCO(3)(-) (24 meq, bubbled with 5% CO(2)), however, the V(h,ACh) was not blocked by bumetanide, but it was suppressed by ethylisopropylamiloride (EIPA), a Na(+)/H(+) exchanger (NHE) inhibitor.	Bicarbonates	19-28	acyl-CoA thioesterase 12	Rattus norvegicus	79-82	
15539434-7	2005	Without HCO(3)(-), an application of ACh strongly accelerated the NKCC activity that was measured from the decay of pH(i) during the application of NH(4)(+) (20 mM).	Bicarbonates	8-14	acyl-CoA thioesterase 12	Rattus norvegicus	37-40	
15539434-8	2005	Notably, the ACh-induced activation of NKCC was largely suppressed in the presence of HCO(3)(-).	Bicarbonates	86-92	acyl-CoA thioesterase 12	Rattus norvegicus	13-16	
15539434-11	2005	The regulation of NKCC and NHE by ACh is strongly affected by the physiological level of HCO(3)(-).	Bicarbonates	89-95	acyl-CoA thioesterase 12	Rattus norvegicus	34-37	
10505751-4	1999	The responses of bicarbonate secretion to intravenous infusion of CCK, acetyl-beta-methylcholine (Ach), and 2-deoxy-D-glucose (2DG), and to intraduodenal infusion of HCl and a liquid meal were examined.	Bicarbonates	17-28	acyl-CoA thioesterase 12	Rattus norvegicus	71-96