Localization of Components of the Renin-Angiotensin System within the Kidney and Sustained Release of Angiotensins from Isolated and Perfused Kidney.

Inagami, Tadashi; Mizuno, Kenji; Kawamura, Minoru; Okamura, Tomio; Clemens, Daniel L.; Higashimori, Koichi

doi:10.1620/tjem.166.17

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…It has traditionally been assumed that angiotensin II inhibits renin production by a direct action on the juxtaglomerular cells (40,41). However, a recent study by Matsusaka et al (42) in chimeric mice carrying a regional null mutation of the angiotensin type 1A (AT 1a ) receptor, the AT 1 receptor subtype exclusively present in mouse jg cells, has questioned whether angiotensin II does act directly on juxtaglomerular cells.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Cheng¹,

Wang²,

Zhang³

et al. 1999

J. Clin. Invest.

197

199

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We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a -/-,Agtr1b -/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Cheng¹,

Wang²,

Zhang³

et al. 1999

J. Clin. Invest.

197

199

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show abstract

“…hemodynamics (7,22,28). It has traditionally been assumed that angiotensin II inhibits renin production by a direct action on JG cells (41,47). However, studies in chimeric mice carrying "regional" null mutation of the angiotensin type 1a (AT 1a ) receptor, the AT 1 receptor subtype exclusively present in mouse JG cells, have questioned whether angiotensin II does act directly on JG cells (63).…”

Section: Cox-2 Expression In the Renal Cortexmentioning

confidence: 99%

Physiological regulation of cyclooxygenase-2 in the kidney

Harris

Breyer

2001

American Journal of Physiology-Renal Physiology

267

251

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In adult mammalian kidney, cyclooxygenase-2 (COX-2) expression is found in a restricted subpopulation of cells. The two sites of renal COX-2 localization detected in all species to date are the macula densa (MD) and associated cortical thick ascending limb (cTALH) and medullary interstitial cells (MICs). Physiological regulation of COX-2 in these cellular compartments suggests functional roles for eicosanoid products of the enzyme. COX-2 expression increases in high-renin states (salt restriction, angiotensin-converting enzyme inhibition, renovascular hypertension), and selective COX-2 inhibitors significantly decrease plasma renin levels, renal renin activity, and mRNA expression. There is evidence for negative regulation of MD/cTALH COX-2 by angiotensin II and by glucocorticoids and mineralocorticoids. Conversely, nitric oxide generated by neuronal nitric oxide synthase is a positive modulator of COX-2 expression. Decreased extracellular chloride increases COX-2 expression in cultured cTALH, an effect mediated by increased p38 mitogen-activated protein kinase activity, and, in vivo, a sodium-deficient diet increases expression of activated p38 in MD/cTALH. In contrast to COX-2 in MD/cTALH, COX-2 expression increases in MICs in response to a high-salt diet as well as water deprivation. Studies in cultured MICs have confirmed that expression is increased in response to hypertonicity and is mediated, at least in part, by nuclear factor-kappaB activation. COX-2 inhibition leads to apoptosis of MICs in response to hypertonicity in vitro and after water deprivation in vivo. In addition, COX-2 metabolites appear to be important mediators of medullary blood flow and renal salt handling. Therefore, there is increasing evidence that COX-2 is an important physiological mediator of kidney function.

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“…number of granules) were of the same order of magnitude in other species such as rat, rabbit and dog (e.g. Taugner et al 1981;Inagami et al 1992;Peti-Peterdi et al 2004). …”

Section: Individual Jga and Plasma Modulesmentioning

confidence: 69%

A Computational Model of the Circulating Renin-Angiotensin System and Blood Pressure Regulation

Guillaud

Hannaert

2010

Acta Biotheor

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(1) model BP, PRA and [Ang II] are within reported ranges, and respond physiologically to sodium intake; (2) short-term Ang II infusion induces reported rise in BP and PRA. The modeled circulating RAS, in interaction with an integrated CVR, exhibits a realistic response to BP control maneuvers. This construction will allow for modelling hypertensive and CVR patients, including salt-sensitivity, polymorphisms, and pharmacotherapeutics.

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Localization of Components of the Renin-Angiotensin System within the Kidney and Sustained Release of Angiotensins from Isolated and Perfused Kidney.

Cited by 9 publications

References 18 publications

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression

Physiological regulation of cyclooxygenase-2 in the kidney

A Computational Model of the Circulating Renin-Angiotensin System and Blood Pressure Regulation

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