Cholera toxin but not pertussis toxin inhibits angiotensin II-enhanced contractions in the rat portal vein.
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.
Department of Pharmacotherapy, University of Amsterdam, Netherlands.
J
J
Zhang
J C
JC
Van Meel
M
M
Pfaffendorf
P A
PA
Van Zwieten
D000262:Adenylyl Cyclases / Q000378:metabolism; D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002772:Cholera Toxin / Q000494:pharmacology*; D019204:GTP-Binding Proteins / Q000378:metabolism; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D037342:Pertussis Toxin; D011169:Portal Vein / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*
D010566:Virulence Factors, Bordetella; D000804:Angiotensin II; D003994:Bucladesine; D002772:Cholera Toxin; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins; D000262:Adenylyl Cyclases