PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8712453-0	1996	Effects of halothane and isoflurane on bradykinin-evoked Ca2+ influx inbovine aortic endothelial cells.	Isoflurane	25-35	kininogen 1	Bos taurus	39-49	
8916833-6	1996	Although basal [Ca2+]i was unaltered by the anesthetics, both halothane and enflurane, in a dose-dependent manner, depressed the peak and plateau of the [Ca2+]i transient elicited by 10 nM bradykinin, whereas isoflurane had no effect.	Isoflurane	209-219	kininogen 1	Bos taurus	189-199	
8712453-4	1996	METHODS: The effect of halothane and isoflurane on the Ca2+ response to bradykinin of bovine aortic endothelial (BAE) cells was investigated using the fluorescent Ca2+ indicator fura-2.	Isoflurane	37-47	kininogen 1	Bos taurus	72-82	
8712453-10	1996	RESULTS: The results of the current study indicate that the initial Ca2+ increase in response to bradykinin stimulation is not affected by halothane, but that pulse applications of halothane (0.4-2 mM) or isoflurane (0.5-1 mM) reversibly reduce the sustained cytosolic Ca2+ increase initiated either by bradykinin or by the Ca2+ pump inhibitor thapsigargin.	Isoflurane	205-215	kininogen 1	Bos taurus	303-313	
8712453-14	1996	CONCLUSIONS: These observations suggest that the effects of halothane and isoflurane on Ca2+ homeostasis in BAE cells reflect, for the most part, a reduction of the thapsigargin- or bradykinin-evoked Ca2+ influx, which would be consequent to a cellular depolarization caused by an inhibition of the Ca(2+)-dependent K+ channel activity initiated after cell stimulation.	Isoflurane	74-84	kininogen 1	Bos taurus	182-192