Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Cheng, Hao; Wang, Junling; Zhang, Mingzhi; Miyazaki, Yoichi; Ichikawa, Iekuni; McKanna, James A.; Harris, Raymond C.

doi:10.1172/jci5505

Cited by 196 publications

(222 citation statements)

References 51 publications

(74 reference statements)

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“…Our data now show that in the absence of calcineurin inhibitors low-salt diet and a combination of low-salt diet with an ACE inhibitor increase renin secretion as well as renin-and COX-2 mRNA expression in parallel, which is in accordance with previous studies (7,8,25). In the presence of CsA, low-salt diet and the combination of low-salt diet and ACE inhibitor stimulates renin secretion and renin expression, whereas Figure 8.…”

Section: Discussionsupporting

confidence: 93%

“…The data obtained in this study clearly demonstrate that calcineurin inhibitors not only decrease basal COX-2 gene expression in the renal cortex and medulla of rats but also attenuate the well-established noninflammatory induction of renocortical COX-2 expression, particularly in the TALH/macula densa structures, by low-salt diet or AngII antagonists (2,7,8). Inhibition of COX-2 gene expression was associated by a decline of COX-2 protein expression as well as by a fall of tissue PGE 2 levels.…”

Section: Discussionsupporting

confidence: 54%

“…Due to the close vicinity of macula densa cells to the reninproducing juxtaglomerular cells, it has been hypothesized that COX-2-derived prostanoids could be involved in the control of renin secretion and renin gene expression (25). This concept has been supported by data obtained from experiments with certain COX-2 blockers (7,45,46) and with COX-2 knockout mice (47,48). However, conflicting data have also been recently reported, raising some doubts on this concept, because commonly available COX-2 blockers do not consistently influence the control of renin synthesis and secretion (31,44,49).…”

Section: Discussionmentioning

confidence: 95%

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Cyclosporine A Suppresses Cyclooxygenase-2 Expression in the Rat Kidney

Höcherl¹,

Dreher²,

Vitzthum

et al. 2002

Journal of the American Society of Nephrology

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Abstract. On the basis of recent evidence that the cyclooxygenase-2 (COX-2) gene promoter contains functional binding sites for the nuclear factor of activated T cells (NFAT) and that COX-2 is expressed in a regulated fashion in the kidney, this study aimed to assess the effect of immunosuppressants on COX-2 expression in the kidney. Therefore, Wistar-Kyoto rats were treated with cyclosporine A (CsA; 15 mg/kg per day) or tacrolimus (5 mg/kg per day) for 7 d each. Both drugs markedly lowered COX-2 expression while COX-1 expression remained unaltered. Furthermore, CsA blunted the increase of renocortical COX-2 expression in response to low salt intake or a combination of low-salt diet with the ACE inhibitor ramipril (10 mg/kg per day), which strongly stimulates renocortical COX-2 expression. At the same time, calcineurin inhibitors moderately enhanced basal as well as stimulated renin secretion and renin gene expression. These findings suggest that inhibition of calcineurin could be a crucial determinant for the regulated expression of COX-2 in the kidney. Inhibition of COX-2 expression may therefore at least in part account for the well-known adverse effects of immunosuppressants in the kidney. Moreover, our data suggest that the stimulation of the renin system by low salt and by ACE inhibitors is not essentially mediated by COX-2 activity.The family of cyclooxygenases (COX)

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 95%

See 1 more Smart Citation

Cyclosporine A Suppresses Cyclooxygenase-2 Expression in the Rat Kidney

Höcherl¹,

Dreher²,

Vitzthum

et al. 2002

Journal of the American Society of Nephrology

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“…This phenomenon is probably a feedback response to the low renin, because decreased renin and angiotensin II levels should lead to decreased angiotensin II-mediated inhibition of COX-2 (36). What, then, is causing the renin to be low?…”

Section: Discussionmentioning

confidence: 99%

Functional expression of the olfactory signaling system in the kidney

Pluznick

Zou

Zhang

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

191

209

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Olfactory-like chemosensory signaling occurs outside of the olfactory epithelium. We find that major components of olfaction, including olfactory receptors (ORs), olfactory-related adenylate cyclase (AC3) and the olfactory G protein (Golf), are expressed in the kidney. AC3 and Golf colocalize in renal tubules and in macula densa (MD) cells which modulate glomerular filtration rate (GFR). GFR is significantly reduced in AC3 ؊/؊ mice, suggesting that AC3 participates in GFR regulation. Although tubuloglomerular feedback is normal in these animals, they exhibit significantly reduced plasma renin levels despite up-regulation of COX-2 expression and nNOS activity in the MD. Furthermore, at least one member of the renal repertoire of ORs is expressed in a MD cell line. Thus, key components of olfaction are expressed in the renal distal nephron and may play a sensory role in the MD to modulate both renin secretion and GFR.adenylate cyclase 3 ͉ glomerular filtration rate ͉ Golf ͉ macula densa ͉ renin

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“…12 In addition, an attenuation of COX-2 expression in rat renal cortex by Ang II was observed. 13,14 Worth noting, in aorta from spontaneously hypertensive rats, an animal model of oxidative stress, increased ROS production was shown to activate COX-1 leading to the production of endoperoxides, which, in turn, stimulate TP receptors on vascular smooth muscle cells. 8 Based on these findings, ROS might be hypothesized as a mechanism whereby Ang II interacts with the COX pathway to induce endothelial dysfunction.…”

mentioning

confidence: 99%

Cyclooxygenase-1 Is Involved in Endothelial Dysfunction of Mesenteric Small Arteries From Angiotensin II–Infused Mice

et al. 2007

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Abstract-Angiotensin II induces endothelial dysfunction by reducing NO availability and increasing reactive oxygen species. We assessed whether cyclooxygenase (COX)-1 or COX-2 participate in the angiotensin II-induced endothelial dysfunction in murine mesenteric small arteries and examined the role of reduced nicotinamide-adenine dinucleotide phosphate-dependent reactive oxygen species production. Mice received angiotensin II (600 ng/kg per minute, SC), saline (controls), angiotensin II ϩ apocynin (reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor, 2.5 mg/day), or apocynin alone for 2 weeks. Endothelial function of mesenteric arteries was assessed by pressurized myograph. In controls, acetylcholine-induced relaxation was inhibited by N G -monomethyl-L-arginine and unaffected by DFU (COX-2 inhibitor), SC-560 (COX-1 inhibitor), or ascorbic acid. In angiotensin II-infused animals, the attenuated response to acetylcholine was less sensitive to N G -monomethyl-L-arginine, unaffected by DFU, and enhanced by SC-560 and, similarly, by SQ-29548, a thromboxane-prostanoid receptor antagonist. Moreover, response to acetylcholine was unchanged by ozagrel, a thromboxane synthase inhibitor, and normalized by ascorbic acid. Apocynin prevented the angiotensin II-induced vascular dysfunctions. In angiotensin II-infused mice, RT-PCR analysis showed a significant COX-2 downregulation, whereas COX-1 expression was upregulated. These changes were unaffected by apocynin. Modulation of COX isoform by angiotensin II was also documented by immunohistochemistry. In small mesenteric vessels, the reduced NO availability and oxidant excess, which characterize endothelial dysfunction secondary to angiotensin II, are associated with a reduced COX-2 and an increased COX-1 function and expression. Angiotensin II causes an oxidative stress-independent COX-1 overexpression, whereas angiotensin II-mediated oxidant excess production stimulates COX-1 activity to produce a contracting prostanoid endowed with agonist activity on thromboxane-prostanoid receptors. Key Words: angiotensin II Ⅲ microcirculation, cyclooxygenase Ⅲ endothelium Ⅲ oxidative stress I t is widely accepted that angiotensin (Ang) II is greatly implicated in the development of endothelial dysfunction in small resistance arteries, 1,2 mainly through an increased generation of reactive oxygen species (ROS) via vascular reduced nicotinamide-adenine dinucleotide phosphate [NAD(P)H] oxidase activation. [3][4][5][6] Mesenteric arteries from Ang II-infused mice are characterized by a blunted endothelium-dependent relaxation, as a consequence of a reduced NO availability because of oxidant excess. 5 Recent evidence indicates that another pathway involved in endothelial dysfunction is cyclooxygenase (COX) activity. Thus, prostaglandins (PGs) have been shown to play a major role in modulating vascular tone, and COX represents a key enzyme in PG synthesis. Indeed, COX metabolizes arachidonic acid into the unstable intermediate PGH 2 , which, in turn, is converted by an array...

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Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Cited by 196 publications

References 51 publications

Cyclosporine A Suppresses Cyclooxygenase-2 Expression in the Rat Kidney

Cyclosporine A Suppresses Cyclooxygenase-2 Expression in the Rat Kidney

Functional expression of the olfactory signaling system in the kidney

Cyclooxygenase-1 Is Involved in Endothelial Dysfunction of Mesenteric Small Arteries From Angiotensin II–Infused Mice

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