Angiotensin administration stimulates renal 11β-hydroxysteroid dehydrogenase activity in healthy men

Kerstens, Michiel N.; Kleij, Frank G.H. van der; Boonstra, A. H.; Sluiter, Wim J.; Molen, J.C. van der; Navis, Gerjan; Dullaart, Robin P. F.

doi:10.1111/j.1523-1755.2004.00626.x

Cited by 6 publications

(3 citation statements)

References 31 publications

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“…Therefore, inulin clearance was measured to evaluate rats' GFR in the presence or absence of AngII with or without TRPC1 inhibition. In agreement with other studies (14,15), infusion of AngII (1.7 ng/min per 100 g body wt) significantly reduced GFR from 2.7 Ϯ 0.6 of basal level to 1.4 Ϯ 0.3 ml/min per 100 g body wt (Figure 2A, normal), representing 42 Ϯ 10% decrease ( Figure 2B, normal). Inclusion of a TRPC1 antibody (polyclonal rabbit IgG, 300 ng/ml), which is directed to an extracellular epitope (predicted pore region) of TRPC1, into perfusate did not alter the basal GFR.…”

Section: Trpc1 Regulated Glomerular Filtration In Ratssupporting

confidence: 79%

Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

Sours-Brothers

Coleman

et al. 2007

Journal of the American Society of Nephrology

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Contractility of mesangial cells (MC) is tightly controlled by [G lomerular mesangial cells (MC) are located within glomerular capillary loops and contribute to the physiologic regulation of glomerular hemodynamics (1). Altered responsiveness of MC to hormones is one of the major causes that lead to various renal diseases. Ca 2ϩ influx across the plasma membrane is a major component of MC responses to vasoconstrictors (1). Several types of Ca 2ϩ -conductive channels in the plasma membrane are involved in the physiologic processes. These channels include voltage-operated Ca 2ϩ channel (VOCC), receptor-operated channel (ROC), and recently found store-operated channel (SOC) (1,2). In contrast to the widely known VOCC, the molecular identity, physiologic significance, and regulatory mechanism of ROC and SOC in the glomerular contractile cells remain unknown.Recently, the channel proteins from a new family, canonical transient receptor potential (TRPC), were found in a variety of cells (3). TRPC family includes seven related members, designated as TRPC1 through 7 (3). Pharmacologic and electrophysiologic studies in conjunction with molecular biologic tools and Ca 2ϩ imagings have demonstrated that TRPC channel activity is tightly linked to the signaling cascade of G protein-coupled receptor or receptor tyrosine kinase (4,5), supporting the current hypothesis that TRPC proteins are potential candidates for ROC and SOC. TRPC proteins have been identified in glomeruli and glomerular MC (6 -8). Our previous work also demonstrated that human MC selectively express TRPC1,3,4, and 6 (9). However, the function, regulation, and physiologic relevance of these glomerular TRPC are unexplored at large extent. In this study, we focused on TRPC1 and investigated its contribution to mesangial contraction in vitro and in vivo. Our results indicate that TRPC1 is an important component mediating contractile responses of MC. The TRPC1-involved mesangial contraction is attributed to TRPC1-associated Ca 2ϩ influx. Materials and Methods AnimalsTwo-to 3-mo-old male Sprague-Dawley rats were used in this study. All rats were purchased from Harlan (Indianapolis, IN). Care and use of all animals in this study were in strict agreement with the guidelines set forth by the University of North Texas Health Science Center. Measurement of GFR and Renal Blood FlowGFR and renal blood flow (RBF) were estimated by measurement of inulin and para-aminohippurate (PAH) plasma clearances as described

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Section: Trpc1 Regulated Glomerular Filtration In Ratssupporting

confidence: 79%

Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

Sours-Brothers

Coleman

et al. 2007

Journal of the American Society of Nephrology

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“…To this purpose, SS was defined as a sodium-induced rise in MAP of >3 mm Hg/150 mmol Na + , as used before, 17 and shown to be reproducible (Cohen's κ = 0.87). 18 In our setting, 15 repeated assessment of SS in healthy young males was reproducible with a Cohen's κ of 0.75 and a correlation of r = 0.641 (P < 0.01) for the individual subjects (unpublished data).…”

Section: Methodsmentioning

confidence: 99%

Renal Response to Angiotensin II is Blunted in Sodium-sensitive Normotensive Men

Visser

Boonstra

Lely

et al. 2008

American Journal of Hypertension

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“…In vitro studies have reported an inhibitory effect of Ang II on 11β-HSD2 activity via the AT 2 receptor [37], while infusion of Ang II in humans increased 11β-HSD2 activity [38]. Because Ang II is a potent stimulator of reactive oxygen species [30], it could also affect 11β-HSD activity by altering the availability of NADP(H) and/or NAD.…”

Section: Elements Of the Intrarenal Raasmentioning

confidence: 99%

Role of the Intrarenal Renin-Angiotensin-Aldosterone System in Chronic Kidney Disease

Siragy

Carey²

2010

Am J Nephrol

233

173

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The existence of local or tissue-based renin-angiotensin-aldosterone systems (RAAS) is well documented and has been implicated as a key player in the pathogenesis of cardiovascular and renal diseases. The kidney contains all elements of the RAAS, and intrarenal formation of angiotensin II not only controls glomerular hemodynamics and tubule sodium transport, but also activates a number of inflammatory and fibrotic pathways. Experimental and clinical studies have shown that the intrarenal RAAS is activated early in diabetic nephropathy, the leading cause of chronic kidney disease (CKD). Although angiotensin-converting enzyme inhibitors and angiotensin receptor blockers decrease the rate of decline in kidney function in patients with diabetic and non-diabetic nephropathy, many patients still progress to end-stage renal disease or die from cardiovascular events. There is still a clear need for additional strategies to block the RAAS more effectively to reduce progression of CKD. The focus of this paper is to review the importance of the intrarenal RAAS in CKD and recent findings in renin-angiotensin biology pertinent to the kidney. We also discuss additional strategies to inhibit the RAAS more effectively and the potential impact of direct renin inhibition on the prevention and management of CKD.

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Angiotensin administration stimulates renal 11β-hydroxysteroid dehydrogenase activity in healthy men

Cited by 6 publications

References 31 publications

Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

Renal Response to Angiotensin II is Blunted in Sodium-sensitive Normotensive Men

Role of the Intrarenal Renin-Angiotensin-Aldosterone System in Chronic Kidney Disease

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