Cholecystokinin-stimulated pepsinogen secretion and cholecystokinin receptors on gastric chief cells in guinea pigs.

نویسندگان

  • M Noguchi
  • H Adachi
  • S Sato
  • T Honda
  • S Ohnishi
  • E Aoki
  • K Torizuka
چکیده

We investigated cholecystokinin (CCK) receptors on isolated gastric chief cells from guinea pig. CCK stimulated pepsinogen secretion from chief cells at the same efficacy as that induced by carbamylcholine. Binding of 125I-labeled CCK-33 (125I-CCK) to chief cells was temperature-dependent, and was saturable and reversible at 37 degrees C. Hofstee plots of the ability of CCK-8 to inhibit binding of 125I-CCK showed a linear regression line, suggesting that CCK receptors possessed one binding site. The dissociation constant of the binding site was calculated to be 3.8 x 10(-10) M. The dose-response curve of CCK for pepsinogen secretion was superimposed on that for the binding to its receptors. These results indicated that gastric chief cells from the guinea pig possess CCK receptors that relate closely to the action of CCK involved in pepsinogen secretion.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Interaction between the calcium and adenylate cyclase messenger systems in dispersed chief cells from guinea pig stomach. Possible cellular mechanism for potentiation of pepsinogen secretion.

To determine the role of the adenylate cyclase system in potentiation of enzyme secretion, we used cholera toxin to activate adenylate cyclase before examining the effects of agents on chief cell cAMP and pepsinogen secretion. Dispersed chief cells were obtained from guinea pig stomach by fractionation of mucosal cells on a Percoll gradient. Incubation of cells with 100 nM cholera toxin for 90 ...

متن کامل

Cholinergic agonist-induced pepsinogen secretion from murine gastric chief cells is mediated by M1 and M3 muscarinic receptors.

Muscarinic cholinergic mechanisms play a key role in stimulating gastric pepsinogen secretion. Studies using antagonists suggested that the M3 receptor subtype (M3R) plays a prominent role in mediating pepsinogen secretion, but in situ hybridization indicated expression of M1 receptor (M1R) in rat chief cells. We used mice that were deficient in either the M1 (M1R-/-) or M3 (M3R-/-) receptor or...

متن کامل

Visualization of cytosolic free calcium distribution and mobilization in guinea pig gastric chief cells.

Distribution and temporal change of free calcium concentration [( Ca2+]i) in single guinea pig gastric chief cells were visualized by a digital imaging microscope equipped with a microspectrofluorometer. The distribution was not homogeneous; a higher [Ca2+]i area was often localized in some restricted regions of the endoplasm and also at the peripheral cytoplasm just beneath the plasma membrane...

متن کامل

Cholecystokinin receptor antagonism of stimulated pancreatic and gastric secretion.

The effects of cholecystokinin receptor antagonist, dipentyl-3,4-dichloroproglumide (DDP), on stimulated pancreatic and gastric secretion were studied in the rat. DDP dose-dependently inhibited cholecystokinin-stimulated amylase release from dispersed acinar cells. In vivo, DDP inhibited cholecystokinin octapeptide-stimulated amylase and protein secretion. DDP also inhibited pentagastrin-stimul...

متن کامل

Lithocholyltaurine interacts with cholinergic receptors on dispersed chief cells from guinea pig stomach.

Although bile acids damage gastric mucosa, the mechanisms underlying tissue injury induced by these agents are not well understood. To determine whether bile acids alter gastric secretory function, we investigated the actions of sodium cholate, deoxycholate, lithocholate, and their taurine and glycine conjugates on a highly homogeneous population of gastric chief cells. Lithocholyltaurine (LCT)...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Endocrinologia japonica

دوره 34 5  شماره 

صفحات  -

تاریخ انتشار 1987