Abstract
Somatostatin and its analogue SMS 201-995 inhibit high voltage-activated (HVA) Ca2+ currents in the rat insulinoma cell line RINm5F which stably express cloned human somatostatin receptor subtype 2 (hSSTR2). In contrast, neither somatostatin nor SMS 201-995 suppresses the HVA Ca2+ currents in RINm5F which stably express cloned hSSTR1. These results suggest that somatostatin-induced inhibition of HVA Ca2+ currents is mediated by a specific receptor subtype and that inhibition of calcium influx through HVA Ca2+ channels is one of the mechanisms of SMS 201-995 action on inhibitory processes of hormone secretion and cell proliferation.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Binding, Competitive
-
Calcium Channels / drug effects*
-
Calcium Channels / metabolism
-
Cell Line
-
Colforsin / pharmacology
-
Cyclic AMP / biosynthesis
-
Electrochemistry
-
Guanosine 5'-O-(3-Thiotriphosphate) / pharmacology
-
Humans
-
Octreotide / pharmacology*
-
Rats
-
Receptors, Somatostatin / classification
-
Receptors, Somatostatin / drug effects
-
Receptors, Somatostatin / metabolism*
-
Somatostatin / pharmacology*
-
Virulence Factors, Bordetella / pharmacology
Substances
-
Calcium Channels
-
Receptors, Somatostatin
-
Virulence Factors, Bordetella
-
Colforsin
-
Guanosine 5'-O-(3-Thiotriphosphate)
-
Somatostatin
-
Cyclic AMP
-
Octreotide