Regulation of cholecystokinin secretion in STC-1 cells by nitric oxide.

Published

Journal Article

In the present study we evaluated the effects of agents anticipated to change NO levels on the secretion of cholecystokinin (CCK) from STC-1 cells. After a 15-min treatment with the nitric oxide (NO) generating agent sodium nitroprusside (SNP; 10 microM), a 24% inhibition in basal CCK release and an increase in cellular guanosine 3',5'-cyclic monophosphate (cGMP) levels were noted. By contrast, SNP (10 microM) had no effect on CCK release stimulated by L-phenylalanine (20 mM). Inhibition of NO synthase (NOS) with NG-nitro-L-arginine methyl ester (L-NAME) produced dose-dependent stimulation in CCK release. L-NAME (100-400 microM) also inhibited ATP-sensitive potassium (KATP) channels in cell-attached patches. Pretreatment of cells with disopyramide (200 microM), a KATP channel blocker, blocked L-NAME stimulation of CCK release. After inhibition of potassium channel activity by L-NAME, addition of the nonhydrolyzable cGMP analogue 8-bromo-cGMP (1-2 mM) reactivated potassium channels. NO-generating agents had no effect on channel activity in inside-out membrane patches. It is concluded that NO may serve as an important regulator of basal CCK release.

Full Text

Duke Authors

Cited Authors

  • Mangel, AW; Scott, L; Prpic, V; Liddle, RA

Published Date

  • October 1996

Published In

Volume / Issue

  • 271 / 4 Pt 1

Start / End Page

  • G650 - G654

PubMed ID

  • 8897884

Pubmed Central ID

  • 8897884

International Standard Serial Number (ISSN)

  • 0002-9513

Digital Object Identifier (DOI)

  • 10.1152/ajpgi.1996.271.4.G650

Language

  • eng

Conference Location

  • United States