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Gastric integrity depends upon the balance between aggressive and protective factors.Renin–angiotensin system regulates the blood pressure and body fluids homeostasis.Hypertensive angiotensins I and II augment the acute gastric mucosal injury.Angiotensin-(1-7), the metabolite of angiotensin I, exhibits gastroprotective activity.Prostaglandins, nitric oxide (NO) and sensory nerves mediate gastroprotection by angiotensin-(1-7).Angiotensin II, the main effector of the renin–angiotensin system (RAS), is generated from the precursor angiotensinogen by the actions of renin, angiotensin-converting enzyme, chymase and various peptidases. RAS is essential in the control of blood pressure and body fluid homeostasis but their involvement in the mechanism of the protection of gastric mucosa has not been extensively studied. On the other hand, angiotensin-(1-7) which acts on the Mas receptor, exhibits a potent vasodilatory activity and attenuates the gastric lesions induced by various ulcerogens. In this review, the mechanism of RAS, the antagonists of angiotensin AT1 and AT2 receptors and angiotensin-(1-7) in formation of gastric damage is discussed with possible translating relevance to treatment modalities in the protection against gastric mucosal injury.