| pubmed-article:8381358 | pubmed:abstractText | Angiotensin II (Ang II)-enhanced phasic contractions in the rat portal vein were concentration dependently inhibited by cholera toxin (0.1-10 micrograms/ml) and dibutyryl cyclic AMP (0.1-1 mM), but not by pertussis toxin (1 micrograms/ml), which suggests that Gi is not involved in the Ang II signal transduction pathway. It also seems likely that the effect of cholera toxin is due to its ability to increase cyclic AMP production through Gs. | lld:pubmed |
