The renin-angiotensin system as a primary cause of polyarteritis nodosa in rats

Autor: John J. Mullins, Andrea Thiele, Beate Kuttler, Gerd Lorenz, Joerg Peters, Rainer Rettig, Barbara S. Peters, Oliver Nicolai, Andreas Beineke
Rok vydání: 2009
Předmět:
Male
Pathology
Captopril
Indoles
CD3 Complex
T-Lymphocytes
Blood Pressure
030204 cardiovascular system & hematology
Renin-Angiotensin System
0302 clinical medicine
Cell Movement
Renin
skin and connective tissue diseases
0303 health sciences
integumentary system
Articles
3. Good health
Antibodies
Antinuclear
Molecular Medicine
Rats
Transgenic
Vasculitis
medicine.drug
Mean arterial pressure
medicine.medical_specialty
Antibodies
Antineutrophil Cytoplasmic
03 medical and health sciences
Internal medicine
Weight Loss
Renin–angiotensin system
Necrotizing Vasculitis
Cytochrome P-450 CYP1A1
medicine
Animals
cardiovascular diseases
030304 developmental biology
business.industry
Polyarteritis nodosa
Body Weight
prorenin
Cell Biology
angiotensin
medicine.disease
Angiotensin II
Polyarteritis Nodosa
Rats
polyarteritis nodosa
Blood pressure
Endocrinology
inflammation
business
Zdroj: Journal of Cellular and Molecular Medicine
Peters, B S, Kuttler, B, Beineke, A, Lorenz, G, Thiele, A, Nicolai, O, Rettig, R, Mullins, J J & Peters, J 2010, ' The renin-angiotensin system as a primary cause of polyarteritis nodosa in rats ', Journal of Cellular and Molecular Medicine, vol. 14, no. 6a, pp. 1318-1327 . https://doi.org/10.1111/j.1582-4934.2009.00778.x
ISSN: 1582-1838
DOI: 10.1111/j.1582-4934.2009.00778.x
Popis: Polyarteritis nodosa is a necrotizing vasculitis of medium-sized arteries of unknown origin. Hypertension is present in 30% of patients with polyarteritis nodosa. In those cases, high renin levels are thought to be secondary to renal involvement. The present study was performed to identify causal factors of polyarteritis nodosa. In cyp1a1ren-2 transgenic rats, vasculitis of medium-sized arteries resembling classical polyarteritis nodosa can be induced. In this model, oral administration of indole-3-carbinol (I3C) activates the liver-specific cyp1a1 promoter, leading to prorenin expression in a dose-dependent manner. After the first 6 weeks of chronic induction with 0.125% I3C, the mean arterial pressure reached a plateau of about 170 mmHg. Ten out of 11 I3C-treated rats, which were chronically instrumented with a telemetric device to measure blood pressure, developed polyarteritis nodosa within 10 weeks of I3C treatment. I3C alone or instrumentation alone did not cause polyarteritis nodosa. The angiotensin-converting enzyme inhibitor captopril completely prevented the development of polyarteritis nodosa, indicating that local angiotensin II generation is a pathogenetic factor in this model. The renin–angiotensin system can play a primary role in the development of polyarteritis nodosa in rats.
Databáze: OpenAIRE
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