Mechanisms of progressive renal disease: role of angiotensin II, cyclooxygenase products and nitric oxide (2002)
- Authors:
- USP affiliated authors: ZATZ, ROBERTO - FM ; FUJIHARA, CLARICE KAZUE - FM
- Unidade: FM
- Subjects: ANGIOTENSINA II; ÓXIDO NÍTRICO
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Journal of Hypertension
- Volume/Número/Paginação/Ano: v. 20, Suppl. 3, p. S37-S44, June, 2002
-
ABNT
ZATS, Roberto e FUJIHARA, Clarice Kazue. Mechanisms of progressive renal disease: role of angiotensin II, cyclooxygenase products and nitric oxide. Journal of Hypertension, v. 20, p. S37-S44, 2002Tradução . . Acesso em: 17 abr. 2024. -
APA
Zats, R., & Fujihara, C. K. (2002). Mechanisms of progressive renal disease: role of angiotensin II, cyclooxygenase products and nitric oxide. Journal of Hypertension, 20, S37-S44. -
NLM
Zats R, Fujihara CK. Mechanisms of progressive renal disease: role of angiotensin II, cyclooxygenase products and nitric oxide. Journal of Hypertension. 2002 ; 20 S37-S44.[citado 2024 abr. 17 ] -
Vancouver
Zats R, Fujihara CK. Mechanisms of progressive renal disease: role of angiotensin II, cyclooxygenase products and nitric oxide. Journal of Hypertension. 2002 ; 20 S37-S44.[citado 2024 abr. 17 ] - Role of glomerular hypertension: glomerular hypertrophy and lipid deposition in the genesis of glomerular sclerosis (gs) of experimental diabetes (dm)
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- Effects of an endothelin et receptor antagonist on experimental fk506 induced acute renal dysfunction
- An extremely high dose of losartan affords superior renoprotection in the remnant model
- Chronic inhibition of nuclear factor-kB attenuates renal injury in the 5/6 renal ablation model
- Absence of focal glomerulosclerosis in aging analbuminemic rats
- Discarding the haystack to examine the needles: the potential role of urinary exosome analysis [Editorial]
- Massive albuminuria glomerulosclerosis (gs) by chronic nitric oxide (no) blackade and sodium overload
- Sodium excess aggravates hypertension and renal parenchymal injury in rats with chronic no inhibition
- Glomerular hypertrophy and lipid deposition in the genesis of glomerular sclerosis (gs) of experimental diabetes (dm)
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