PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8381826-1	1993	We demonstrated recently that isoproterenol enhanced the cardiac voltage-dependent sodium currents (INa) in rabbit ventricular myocytes through dual G-protein regulatory pathways.	Isoproterenol	30-43	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	100-103	
8381826-2	1993	In this study, we tested the hypothesis that isoproterenol reverses the sodium channel blocking effects of class I antiarrhythmic drugs through modulation of INa.	Isoproterenol	45-58	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	158-161	
8381826-4	1993	Reversal of lidocaine suppression of INa by isoproterenol (1 microM) was significant at various concentrations of lidocaine (20, 65, and 100 microM, P < 0.05).	Isoproterenol	44-57	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	37-40	
8381826-5	1993	The effects of isoproterenol were voltage dependent, showing reversal of INa suppression by lidocaine at normal and hyperpolarized potentials (negative to -80 mV) but not at depolarized potentials.	Isoproterenol	15-28	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	73-76	
8381826-10	1993	These results suggest that enhancement of INa is an important mechanism by which isoproterenol reverses the effects of class I antiarrhythmic drugs.	Isoproterenol	81-94	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	42-45