CIGARETTE-SMOKE INCREASES GASTRIC-ULCER SIZE IN PART BY AN ANGIOTENSIN II-MEDIATED MECHANISM IN RATS

To assess the mechanism of the effect of cigarette smoke on ulcer dise ase we employed a rat model in which cigarette smoke increases the siz e of acetic acid-induced gastric ulcer and decreases the hyperemia at the ulcer margin. We postulate that cigarette smoke increases angioten sin II (a vasoconstrictor) in ulcer tissue. Since direct measurement o f angiotensin II in small tissue samples is problematic, we compared t he messenger ribonucleic acid (mRNA) for its precursors (angiotensinog en and renin) in ulcer and normal gastric tissue. We also evaluated th e effect of enalapril, which blocks the conversion of angiotensin I to angiotensin II on ulcer size. In the ulcer tissue, cigarette smoke pr oduced a significant increase in mRNA for angiotensinogen but not for renin. Enalapril decreased the size of the gastric ulcer in rats expos ed to cigarette smoke. The data support the possibility that in ulcer tissue cigarette smoke stimulates an angiotensin II-mediated mechanism , which may in part be responsible for the impairment of ulcer margin hyperemia and aggravation of ulcer size.