PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17339532-1	2007	Acute phosphodiesterase 5A inhibition by sildenafil or EMD360527/5 promoted profound inhibition of the cardiac Na(+)/H(+) exchanger (NHE-1), detected by the almost null intracellular pH recovery from an acute acid load (ammonium prepulse) in isolated papillary muscles from Wistar rats.	Sildenafil Citrate	41-51	solute carrier family 9 member A1	Rattus norvegicus	133-138	
33152335-0	2021	PDE5 inhibition improves cardiac morphology and function in SHR by reducing NHE1 activity: Repurposing sildenafil for the treatment of hypertensive cardiac hypertrophy.	Sildenafil Citrate	103-113	solute carrier family 9 member A1	Rattus norvegicus	76-80	
33152335-1	2021	Previously, we have shown that an increased cGMP-activated protein Kinase (PKG) activity after phosphodiesterase 5 (PDE5) inhibition by Sildenafil (SIL), leads to myocardial Na+/H+ exchanger (NHE1) inhibition preserving its basal homeostatic function.	Sildenafil Citrate	136-146	solute carrier family 9 member A1	Rattus norvegicus	192-196	
33152335-5	2021	Compared to their littermate controls, SIL-treated rats presented a decreased NHE1 activity, which correlated with a reduction in its phosphorylation level assigned to activation of a PKG-p38 MAP kinase-PP2A signaling pathway.	Sildenafil Citrate	39-42	solute carrier family 9 member A1	Rattus norvegicus	78-82	
21325817-12	2011	Sildenafil did not reduce the phosphorylated ERK1/2-p90(RSK) levels but blunted NHE-1 phosphorylation suggesting a direct dephosphorylating action.	Sildenafil Citrate	0-10	solute carrier family 9 member A1	Rattus norvegicus	80-85	
21325817-13	2011	CONCLUSIONS: 1) Reperfusion injury would result from ROS-triggered MAPK-mediated NHE-1 phosphorylation (and reactivation) during reperfusion; 2) sildenafil protects the myocardium by favouring NHE-1 dephosphorylation and bypassing ROS generation.	Sildenafil Citrate	145-155	solute carrier family 9 member A1	Rattus norvegicus	81-86	
21325817-13	2011	CONCLUSIONS: 1) Reperfusion injury would result from ROS-triggered MAPK-mediated NHE-1 phosphorylation (and reactivation) during reperfusion; 2) sildenafil protects the myocardium by favouring NHE-1 dephosphorylation and bypassing ROS generation.	Sildenafil Citrate	145-155	solute carrier family 9 member A1	Rattus norvegicus	193-198	
30721701-2	2019	In the heart, Sildenafil was shown to protect against an ischemic insult by decreasing cardiac Na+/H+ exchanger (NHE1) activity, action that was mediated by protein kinase G. p38 mitogen activated protein kinase (p38MAPK) activation was described in cardiac ischemia, but its precise role remains elusive.	Sildenafil Citrate	14-24	solute carrier family 9 member A1	Rattus norvegicus	113-117	
30721701-4	2019	Current study was aimed to seek the role of p38MAPK in the Sildenafil-triggered pathway leading to NHE1 inhibition in myocardium.	Sildenafil Citrate	59-69	solute carrier family 9 member A1	Rattus norvegicus	99-103	
30721701-7	2019	Sustained acidosis promoted NHE1 hyperactivity by enhancing Ser703 phosphorylation, effect that was blunted by Sildenafil.	Sildenafil Citrate	111-121	solute carrier family 9 member A1	Rattus norvegicus	28-32	
30721701-8	2019	p38MAPK inhibition reversed the effect of Sildenafil on NHE1.	Sildenafil Citrate	42-52	solute carrier family 9 member A1	Rattus norvegicus	56-60	
30721701-13	2019	Taken together, these results suggest that activation of p38MAPK is a necessary step to trigger the inhibitory effect of Sildenafil on cardiac NHE1 activity, thorough a mechanism that involves protein phosphatase 2A-mediated exchanger dephosphorylation.	Sildenafil Citrate	121-131	solute carrier family 9 member A1	Rattus norvegicus	143-147	
17339532-3	2007	We then tested whether the beneficial effects of NHE-1 inhibitors against the deleterious postmyocardial infarction (MI) remodeling can be detected after sildenafil-mediated NHE-1 inhibition.	Sildenafil Citrate	154-164	solute carrier family 9 member A1	Rattus norvegicus	49-54	
17339532-3	2007	We then tested whether the beneficial effects of NHE-1 inhibitors against the deleterious postmyocardial infarction (MI) remodeling can be detected after sildenafil-mediated NHE-1 inhibition.	Sildenafil Citrate	154-164	solute carrier family 9 member A1	Rattus norvegicus	174-179	
17339532-10	2007	Intracellular pH recovery after an acid load was faster in papillary muscles from post-MI hearts (versus sham), whereas sildenafil significantly inhibited NHE-1 activity in both post-MI and sildenafil-treated sham groups.	Sildenafil Citrate	120-130	solute carrier family 9 member A1	Rattus norvegicus	155-160	
17339532-10	2007	Intracellular pH recovery after an acid load was faster in papillary muscles from post-MI hearts (versus sham), whereas sildenafil significantly inhibited NHE-1 activity in both post-MI and sildenafil-treated sham groups.	Sildenafil Citrate	190-200	solute carrier family 9 member A1	Rattus norvegicus	155-160