Angiotensin type 1 and type 2 receptors during ontogeny: cardiovascular and renal effects

Vinturache, Angela; Smith, Francine G.

doi:10.1016/j.vph.2014.11.001

Cited by 21 publications

(17 citation statements)

References 116 publications

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“…This effect of angiotensin II blockade parallels its well established role in utero where it retards normal fetal kidney growth and development. 10 Is this report relevant to FSGS as it occurs in man? The mature FSGS lesion in the rat model system was indistinguishable from a human FSGS lesion, and the rat FSGS-associated transcriptomic signature correlated with diverse progressive human glomerular diseases.…”

Section: Discussionmentioning

confidence: 99%

FSGS as an Adaptive Response to Growth-Induced Podocyte Stress

Nishizono

Kikuchi

Wang³

et al. 2017

JASN

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Glomerular sclerotic lesions develop when the glomerular filtration surface area exceeds the availability of podocyte foot process coverage, but the mechanisms involved are incompletely characterized. We evaluated potential mechanisms using a transgenic (podocin promoter-AA-4E-BP1) rat in which podocyte capacity for hypertrophy in response to growth factor/nutrient signaling is impaired. FSGS lesions resembling human FSGS developed spontaneously by 7 months of age, and could be induced earlier by accelerating kidney hypertrophy by nephrectomy. Early segmental glomerular lesions occurred in the absence of a detectable reduction in average podocyte number per glomerulus and resulted from the loss of podocytes in individual glomerular capillary loops. Parietal epithelial cell division, accumulation on Bowman's capsule, and tuft invasion occurred at these sites. Three different interventions that prevented kidney growth and glomerular enlargement (calorie intake reduction, inhibition of mammalian target of rapamycin complex, and inhibition of angiotensin-converting enzyme) protected against FSGS lesion development, even when initiated late in the process. Ki67 nuclear staining and unbiased transcriptomic analysis identified increased glomerular (but not podocyte) cell cycling as necessary for FSGS lesion development. The rat FSGS-associated transcriptomic signature correlated with human glomerular transcriptomes associated with disease progression, compatible with similar processes occurring in man. We conclude that FSGS lesion development resulted from glomerular growth that exceeded the capacity of podocytes to adapt and adequately cover some parts of the filtration surface. Modest modulation of the growth side of this equation significantly ameliorated FSGS progression, suggesting that glomerular growth is an underappreciated therapeutic target for preservation of renal function.

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Section: Discussionmentioning

confidence: 99%

FSGS as an Adaptive Response to Growth-Induced Podocyte Stress

Nishizono

Kikuchi

Wang³

et al. 2017

JASN

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“…Activation of AT 1 R by its native ligand angiotensin II stimulates phospholipase C, production of cyclic adenosine monophosphate, and activation of mitogen-activated protein kinase, which promotes vasoconstriction and hypertension (24). Association between AT 1 R antibody and rejection was first reported in patients with malignant hypertension by Dragun and her colleagues.…”

Section: Antibodies To Micamentioning

confidence: 99%

Impact of Non-Human Leukocyte Antigen-Specific Antibodies in Kidney and Heart Transplantation

Zhang

Reinsmoen

2017

Front. Immunol.

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The presence of donor human leukocyte antigen (HLA)-specific antibodies has been shown to be associated with graft loss and decreased patient survival, but it is not uncommon that donor-specific HLA antibodies are absent in patients with biopsy-proven antibody-mediated rejection. In this review, we focus on the latest findings on antibodies against non-HLA antigens in kidney and heart transplantation. These non-HLA antigens include myosin, vimentin, Kα1 tubulin, collagen, and angiotensin II type 1 receptor. It is suggested that the detrimental effects of HLA antibodies and non-HLA antibodies synergize together to impact graft outcome. Injury of graft by HLA antibodies can cause the exposure of neo-antigens which in turn stimulate the production of antibodies against non-HLA antigens. On the other hand, the presence of non-HLA antibodies may increase the risk for a patient to develop HLA-specific antibodies. These findings indicate it is imperative to stratify the patient’s immunologic risk by assessing both HLA and non-HLA antibodies.

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“…Active renin is released into the circulation and cleaves its only known substrate, angiotensinogen (AGT), which is primarily synthesized in the liver, generating the decapeptide, angiotensin (Ang) I. Ang I is further converted into Ang II by angiotensin-converting enzyme (ACE), which is predominantly expressed on endothelial cells of the pulmonary circulation and the kidney (Cushman & Cheung, 1971; Ryan, Ryan, Whitaker, & Chiu, 1976). Ang II, the major bioactive peptide of the RAS, binds to G-protein-coupled Ang II receptors, including AT 1 R and AT 2 R (Vinturache & Smith, 2014), and contributes to BP regulation as well as the pathogenesis of hypertension by regulating sympathetic activity, vasoconstriction, sodium retention, thirst, and aldosterone synthesis and secretion from the adrenal cortex.…”

Section: Introductionmentioning

confidence: 99%

The critical role of the central nervous system (pro)renin receptor in regulating systemic blood pressure

Jensen

Peng

et al. 2016

Pharmacology & Therapeutics

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The systemic renin–angiotensin system (RAS) has long been recognized as a critically important system in blood pressure (BP) regulation. However, extensive evidence has shown that a majority of RAS components are also present in many tissues and play indispensable roles in BP regulation. Here, we review evidence that RAS components, notably including the newly identified (pro)renin receptor (PRR), are present in the brain and are essential for the central regulation of BP. Binding of the PRR to its ligand, prorenin or renin, increases BP and promotes progression of cardiovascular diseases in an angiotensin II-dependent and -independent manner, establishing the PRR a promising antihypertensive drug target. We also review the existing PRR blockers, including handle region peptide and PRO20, and propose a rationale for blocking prorenin/PRR activation as a therapeutic approach that does not affect the actions of the PRR in vacuolar H+-ATPase and development. Finally, we summarize categories of currently available antihypertensive drugs and consider future perspectives.

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Angiotensin type 1 and type 2 receptors during ontogeny: cardiovascular and renal effects

Cited by 21 publications

References 116 publications

FSGS as an Adaptive Response to Growth-Induced Podocyte Stress

FSGS as an Adaptive Response to Growth-Induced Podocyte Stress

Impact of Non-Human Leukocyte Antigen-Specific Antibodies in Kidney and Heart Transplantation

The critical role of the central nervous system (pro)renin receptor in regulating systemic blood pressure

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