EFFECT OF NICOTINE ON THE ENTEROCHROMAFFIN-LIKE CELLS OF THE OXYNTIC MUCOSA OF THE RAT

Smoking has an unfavourable effect on peptic ulcer disease. The pathop hysiological mechanisms underlying this effect are not known. The ente rochromaffin like (ECL) cell is the cellular source of histamine parti cipating in the regulation of acid secretion. The ECL cell is under fu nctional and trophic control of gastrin and the vagus nerves. Nicotine may affect acid secretion through vagal pathways. Furthermore, nicoti ne may also stimulate neuroendocrine cells.The present study examined if chronic nicotine administration could stimulate the function and gr owth of the ECL cell. Rats inhaled nicotine vapour at a concentration of approximately 6.2 mumol/m3, 20 hours/day, 5 days/week for 11 weeks. Steady state plasma nicotine concentration was 461.8 (137.5 (SD)) nmo l/l. The ECL cell density, histamine content and histidine decarboxyla se activity of the oxyntic mucosa were similar to the controls. We als o examined the effect of acute nicotine stimulation on the acid output and histamine release from the totally isolated vascularly perfused r at stomach. Nicotine did not stimulate acid secretion or histamine rel ease. Thus no evidence could be provided to support the hypothesis tha t nicotine exerts its negative effects on peptic ulcer disease by stim ulating the ECL cell.