[Inhibitory mechanism of experimental stress ulcer in spontaneously hypertensive rats (SHR) from the view point of mucosal blood flow].

Stress ulcer formation is reportedly much less frequent in SHR than in normotensive control rats (Wistar Kyoto Rat: WKY). The purpose of this study was to investigate the mechanism of maintenance of gastric mucosal blood flow (GMBF) during imposed stress in SHR. In stressed-only SHR, GMBF did not significantly change during water immersion and restraint conditions and ulcer index (UI) was significantly lower than that of WKY. Stress conditions led to a fall in blood pressure and a gradual fall in heart rate in WKY and SHR. It was assumed that the changes in blood pressure and heart rate during stress were due to vagal hyperfunction. The catecholamine level in the fundic gland of the gastric tissue was higher in the non-stressed SHR than in the non-stressed WKY. The administration of 6-hydroxydopamine to SHR produced a significant reduction in GMBF during stress conditions and UI was significantly higher in this group than in the stressed-only SHR. In SHR treated with nifedipine, UI was lower than that of the control group and GMBF showed no significant change compared with the stressed-only SHR. However, the administration of verapamil produced a significant reduction in GMBF during stress conditions and increased UI. The norepinephrine and dopamine levels of the groups treated with verapamil were significantly lower than those in the groups treated with nifedipine. These results suggest that local regulation of gastric mucosa mediated by sympathetic hyperfunction in SHR is more important for the maintenance of GMBF during stress conditions than changes in peripheral artery resistance.