Anti-inflammatory effects of angiotensin II AT1 receptor antagonism prevent stress-induced gastric injury

Autor: Gustavo Baiardi, Claudia Bregonzio, Juan M. Saavedra, Hiromichi Ando, Ines Armando, Miroslava Jezova
Rok vydání: 2003
Předmět:
Male
Restraint
Physical
medicine.medical_specialty
Epinephrine
Tyrosine 3-Monooxygenase
Neutrophils
Physiology
Tetrazoles
Biology
Dinoprostone
Receptor
Angiotensin
Type 1
Gastric Content
Angiotensin Receptor Antagonists
Leukocyte Count
Stress
Physiological
Rats
Inbred SHR
Physiology (medical)
Internal medicine
Renin–angiotensin system
Gastric mucosa
medicine
Animals
RNA
Messenger
Stomach Ulcer
Receptors
Angiotensin
Angiotensin II receptor type 1
Hepatology
Tumor Necrosis Factor-alpha
Angiotensin II
Stomach
Biphenyl Compounds
Gastroenterology
Arteries
Intercellular Adhesion Molecule-1
digestive system diseases
Rats
Cold Temperature
Candesartan
medicine.anatomical_structure
Endocrinology
Adrenal Medulla
Gastric Mucosa
Benzimidazoles
Endothelium
Vascular
Corticosterone
Blood Flow Velocity
medicine.drug
Zdroj: American Journal of Physiology-Gastrointestinal and Liver Physiology. 285:G414-G423
ISSN: 1522-1547
0193-1857
DOI: 10.1152/ajpgi.00058.2003
Popis: Stress reduces gastric blood flow and produces acute gastric mucosal lesions. We studied the role of angiotensin II in gastric blood flow and gastric ulceration during stress. Spontaneously hypertensive rats were pretreated for 14 days with the AT1 receptor antagonist candesartan before cold-restraint stress. AT1 receptors were localized in the endothelium of arteries in the gastric mucosa and in all gastric layers. AT1 blockade increased gastric blood flow by 40–50%, prevented gastric ulcer formation by 70–80% after cold-restraint stress, reduced the increase in adrenomedullary epinephrine and tyrosine hydroxylase mRNA without preventing the stress-induced increase in adrenal corticosterone, decreased the stress-induced expression of TNF-α and that of the adhesion protein ICAM-1 in arterial endothelium, decreased the neutrophil infiltration in the gastric mucosa, and decreased the gastric content of PGE2. AT1 receptor blockers prevent stress-induced ulcerations by a combination of gastric blood flow protection, decreased sympathoadrenal activation, and anti-inflammatory effects (with reduction in TNF-α and ICAM-1 expression leading to reduced neutrophil infiltration) while maintaining the protective glucocorticoid effects and PGE2 release. Angiotensin II has a crucial role, through stimulation of AT1 receptors, in the production and progression of stress-induced gastric injury, and AT1 receptor antagonists could be of therapeutic benefit.
Databáze: OpenAIRE
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