Somatostatin receptor subtype SSTR2 mediates the inhibition of high-voltage-activated calcium channels by somatostatin and its analogue SMS 201-995

• Published in: FEBS letters Vol. 355; no. 2; pp. 117 - 120
• Main Authors: Fujii, Yasukazu, Gonoi, Tohru, Yamada, Yuichiro, Chihara, Kazuo, Inagaki, Nobuya, Seino, Susumu
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 28-11-1994
• Subjects: Animals; Binding, Competitive; Calcium Channels - drug effects; Calcium Channels - metabolism; Cell Line; Colforsin - pharmacology; Cyclic AMP - biosynthesis; Electrochemistry; G-protein; Guanosine 5'-O-(3-Thiotriphosphate) - pharmacology; Humans; Intracellular calcium; Octreotide - pharmacology; Rats; Receptors, Somatostatin - classification; Receptors, Somatostatin - drug effects; Receptors, Somatostatin - metabolism; Somatostatin - pharmacology; Somatostatin analogue; Somatostatin receptor subtype; Virulence Factors, Bordetella - pharmacology; Voltage-dependent calcium channel; G-protein; Somatostatin analogue; Somatostatin receptor subtype; Intracellular calcium; Voltage-dependent calcium channel
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/0014-5793(94)01159-1

Somatostatin and its anologue SMS 201-995 inhibit high voltage-activated (HVA) Ca
2+ 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 Ca
2+ currents in RINm5F which stably express cloned hSSTR1. These results suggest that somatostatin-induced inhibition of HVA Ca
2+ currents is mediated by a specific receptor subtype and that inhibition of calcium influx through HVA Ca
2+ channels is one of the mechanisms of SMS 201-995 action on inhibitory processes of hormone secretion and cell proliferation.