Angiotensin II stimulates cyclooxygenase-2 mRNA expression in renal tissue from rats with kidney failure

Hernández, José A.; Astudillo, Horacio; Escalante, Bruno

doi:10.1152/ajprenal.00194.2001

Cited by 21 publications

(17 citation statements)

References 33 publications

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“…This finding suggests uric acid-induced vasculopathy is independent of elevated systemic BP. Additionally, although increased COX-2 expression was reported in arteries from hypertensive rats (35), increased cortical expression of COX-2 induced by renal ablation or angiotensin II infusion has been shown to be BP-independent (36).…”

Section: Discussionmentioning

confidence: 96%

A Role for Uric Acid in the Progression of Renal Disease

Kang

Nakagawa²,

Li³

et al. 2002

Journal of the American Society of Nephrology

1,160

770

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Abstract. Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RKϩOA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 Ϯ 2.5 versus 17.5 Ϯ 3.4%; P Ͻ 0.05) and interstitial fibrosis (1.89 Ϯ 0.45 versus 1.52 Ϯ 0.47; P Ͻ 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhihbitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.

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Section: Discussionmentioning

confidence: 96%

A Role for Uric Acid in the Progression of Renal Disease

Kang

Nakagawa²,

Li³

et al. 2002

Journal of the American Society of Nephrology

1,160

770

View full text Add to dashboard Cite

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“…AngII stimulates PG-endoperoxide synthase 2 (PTGS2) and PG synthesis in the vascular endothelium (Gimbrone & Wayne 1975), renal tissue (Hernández et al 2002), and human monocytes (Kim et al 2005). In rabbit ovaries perfused in vitro, AngII was found to stimulate PGE 2 and PGF 2a production in the absence of gonadotropins (Yoshimura et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

Barreta

Oliveira²,

Ferreira³

et al. 2008

Reproduction

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Angiotensin II (AngII) prevents the inhibitory effect of follicular cells on oocyte maturation, but its involvement in LH-induced meiotic resumption remains unknown. The aim of this study was to assess the involvement of AngII in LH-induced meiotic resumption and of prostaglandins (PGs) in the action of AngII. In the experiment I, seven cows were superovulated, intrafollicularly injected with 10 mM saralasin (a competitive AngII antagonist) or saline when the follicles reached a diameter larger than 12 mm, and challenged with a GnRH agonist to induce an LH surge. Fifteen hours after GnRH, the animals were ovariectomized and the oocytes were recovered to determine the stage of meiosis. The oocytes from follicles that received saline were in germinal vesicle (GV) breakdown (30.8%) or metaphase I (MI; 69.2%) stage while those that received saralasin were in the GV stage (100%; P!0.001) 15 h after GnRH agonist. In another experiment, oocytes were co-cultured with follicular hemisections for 15 h to determine whether PGs mediate the effect of AngII on meiotic resumption. Indomethacin (10 mM) inhibited AngII-induced meiotic resumption (13.4 vs 77.5% MI without indomethacin; P!0.001). Furthermore, the GV oocytes progressed to MI at a similar rate when PGE 2 , PGF 2a or AngII was present in the co-culture system with follicular cells (PGE 2 77.4%, PGF 2a 70.0%, and AngII 75.0% MI). In conclusion, our results provide strong evidence that AngII mediates the resumption of meiosis induced by an LH surge in bovine oocytes and that this event is dependent on PGE 2 or PGF 2a produced by follicular cells. Reproduction (2008) 136 733-740

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“…Cyclooxygenase-2 has been identified as the key player that initiates the cascade of proteolytic activity required for tissue remodeling process during ovulation (Sirois 1994, Sirois & Dore 1997, Robker et al 2000, Peters et al 2004. In some tissues, Ang II induces an increase in expression of cyclooxygenase-2 and prostaglandins (Gimbrone & Wayne Alexander 1975, Hernández et al 2002, Scheuren et al 2002, Kim et al 2005. The action of Ang II in the ovulatory process appears to differ between some species.…”

Section: Introductionmentioning

confidence: 99%

The role of angiotensin II in the early stages of bovine ovulation

Ferreira

Oliveira²,

Fernandes³

et al. 2007

Reproduction

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There is evidence that the renin-angiotensin system plays an important role in ovulation in cattle. Using an in vivo model, we investigated the role of angiotensin (Ang) II in bovine ovulation by injecting Ang II receptor antagonists into ovulatory follicles. Animals (nZ102) were pre-synchronized and, when the follicles reached 12 mm, they were given the respective treatment and the cows received GnRH agonist (i.m.) to induce ovulation. The ovulation rate was significantly lower when 100 mM saralasin (Ang II receptor antagonist) was intrafollicularly injected (14.3%) in comparison with saline solution (83.3%). Based on these results, a second experiment was carried out to determine the timing of Ang II's critical role in ovulation. Saralasin inhibited ovulation only when applied at 0 and 6 h (16.7 and 42.9% ovulation rate in the 0-and 6-h groups respectively), but not at 12 h (100%) following GnRH agonist treatment. To investigate the subtypes of Ang II receptors implicated in the LH-induced ovulation, losartan (LO; AT 1 -Ang II receptor antagonist), PD123 319 (AT 2 -Ang II receptor antagonist), LOCPD123 319, or saline were intrafollicularly injected when the cows were challenged with GnRH agonist. Ovulation was inhibited by PD123 319 and LOCPD123 319 (50.0 and 33.3% on ovulation rate respectively), but not by LO or saline solution (100% ovulation in both groups). From these results, we suggest that Ang II plays a pivotal role in the early mechanism of bovine ovulation via the AT 2 receptor subtype.

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Angiotensin II stimulates cyclooxygenase-2 mRNA expression in renal tissue from rats with kidney failure

Cited by 21 publications

References 33 publications

A Role for Uric Acid in the Progression of Renal Disease

A Role for Uric Acid in the Progression of Renal Disease

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

The role of angiotensin II in the early stages of bovine ovulation

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