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Radiographic evidence of cholecystokinin octapeptide receptors in the hamster gallbladder
108 RELATIONSHIP BETWEEN HYPERFUNCTION OF ANTRAL G CELLS (AGCH) AND AUTONOMIC NEUROPATHY (AN) IN DIABETIC PATIENTS. B.Annlbale, M.G.Felici*, V.Spallone*, M.R. Maiello,, V.Corleto, G.Menzinger*, G.F.DelIe Fare. Gastroenterology Unit University "La Sapienza", *Metabolic Disease,Dept.lnt.Med., University "Tor Vergata", Rome, Italy. It has been reported in diabetic patients the occurence of basal and mealstimulated hypergastrinemia. Gastrin release is under vagal control, i.e. vagotomy increases gastrin levels. The aim of our study was to evaluate the infuence of autonomic neuropathy (AN) on gastrin release in diabetic patients and the related effects of the hypergastrinemia. We have studied 21 diabetics with AN, 19 without AN and 21 normal subjects. The three groups studied were comparable for age, duration of diabetes and sex. AN were evaluated by using cardiovascular tests (beat to beat variation, lying to standing, Valsalva manoeuvre, postural hypotension). Serum gastrin levels were measured by specific RIA basally (n.v.:50-150 pg/ml) and after a protein-rich meal (n.v.:150-350). Upper endoscopy and ultrasonography gastric emptying were also performed. A great proportion (11/21) of neuropatics showed a pathological gastrin peak increase after meal; the same result was obtained in 6/19 non-neuropatics. However, only diabetic patients with AN had gastrin peak levels significantly higher (p<0.01) than controls. A linear correlation between the score of AN and peak gastrin levels (r=0.43; p<0.01) has been found. BAO and PAO values were in the lower normal range. No patients had chronic gastritis atrophy type A. No evidence of gastric stasis was observed, the 50% of the patients showed a delayed gastric emptying, irrespective to the presence of AN. Gastric vagal neuropathy affects a large proportion of diabetic patients causing an hyperfunctionof antral G cells. An effective vagal gastric damage is also suggested by the lack of acid hypersecretion in response to hypergastrinemia.
RADIOGRAPHIC EVIDENCE OF CHOLECYSTOK/NIN OCTAPEPTIDE RECEPTORS IN THE HAMSTER GALLBLADDER. Aoki T, Ueno T, Toyonaga A, Sakata R, Kimura Y, Minetoma T, Inuzuka S, Torimura T, Sasaki E & Tanikawa K. Second Dept. of Medicine, Kurume University School of Medicine, 67 Asahi-machi Kurume, Fukuoka 830, Japan. [ Aim] The present study was undertaken to clarify the relationship between smooth muscle cells and cholecystokinin-receptor (CCKr) in the muscle layer of hamster gallbladder (GB) using light and ~ectron microscopic autoradiography. [MethodJ Male golden hamsters (14-22 weeks) were used : 1) Light and electron microscopy: GB sections were observed after fixation by 2% formaldehyde-2.5% glutaraldehyde. 2) Light and electron microscopic~2sautoradiography : GB sections were incubated" for 40 minutes with a radiolabeled I-Boton-Hunter CCK-octapeptide (I-CCK), and were dipped in autoradiography emulsion. The autoradiograms were developed with Konidol X (Konica), and observed under light and electron microscope. [ Result] The distribution of I-CCK in the gallbladder : 1) Light microscopy : Remarkable accumulation of radiolabeled CCK was observed at sites corresponding to the GB muscle layers. 2) Electron microscopy : The localization of radiolabeled CCK was revealed corresponding to the cell membrane of smooth muscle cells in the muscle layer. Furthermore, radiolabeled CCK was observed on the cell membrane near cell-to-cell junctions. [Conclusion ] GB contraction is considered to be produced primarily by direct action of CCK, which penetrates into the GB tissue by way of the blood flow of capillaries and combines with its receptors of smooth muscle cells. However, the presence of a small number of myoneural junctions suggests an involvement of cholinergic nerves. The contractility of GB is considered to be adjusted through cell-to-cell junctions, and to be effective for discharge of bile.
RADIOGRAPHIC EVIDENCE OF CHOLECYSTOK/NIN OCTAPEPTIDE RECEPTORS IN THE HAMSTER GALLBLADDER. Aoki T, Ueno T, Toyonaga A, Sakata R, Kimura Y, Minetoma T, Inuzuka S, Torimura T, Sasaki E & Tanikawa K. Second Dept. of Medicine, Kurume University School of Medicine, 67 Asahi-machi Kurume, Fukuoka 830, Japan. [ Aim] The present study was undertaken to clarify the relationship between smooth muscle cells and cholecystokinin-receptor (CCKr) in the muscle layer of hamster gallbladder (GB) using light and ~ectron microscopic autoradiography. [MethodJ Male golden hamsters (14-22 weeks) were used : 1) Light and electron microscopy: GB sections were observed after fixation by 2% formaldehyde-2.5% glutaraldehyde. 2) Light and electron microscopic~2sautoradiography : GB sections were incubated" for 40 minutes with a radiolabeled I-Boton-Hunter CCK-octapeptide (I-CCK), and were dipped in autoradiography emulsion. The autoradiograms were developed with Konidol X (Konica), and observed under light and electron microscope. [ Result] The distribution of I-CCK in the gallbladder : 1) Light microscopy : Remarkable accumulation of radiolabeled CCK was observed at sites corresponding to the GB muscle layers. 2) Electron microscopy : The localization of radiolabeled CCK was revealed corresponding to the cell membrane of smooth muscle cells in the muscle layer. Furthermore, radiolabeled CCK was observed on the cell membrane near cell-to-cell junctions. [Conclusion ] GB contraction is considered to be produced primarily by direct action of CCK, which penetrates into the GB tissue by way of the blood flow of capillaries and combines with its receptors of smooth muscle cells. However, the presence of a small number of myoneural junctions suggests an involvement of cholinergic nerves. The contractility of GB is considered to be adjusted through cell-to-cell junctions, and to be effective for discharge of bile.