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Am J Physiol Gastrointest Liver Physiol 271: G650-G654, 1996;
0193-1857/96 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 271, Issue 4 650-G654, Copyright © 1996 by American Physiological Society

ARTICLES

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

A. W. Mangel, L. Scott, V. Prpic and R. A. Liddle
Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.

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.


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