angiotensin/atrophy

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Uric acid and allograft loss from interstitial fibrosis/tubular atrophy: post hoc analysis from the angiotensin II blockade in chronic allograft nephropathy trial.

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BACKGROUND Uric acid has been linked to the progression of native kidney disease. Studies evaluating its contribution to allograft function in kidney transplant recipients, among whom hyperuricemia is common, have yielded mixed results. METHODS We evaluated the association between baseline uric acid

Observational Study of Brain Atrophy and Cognitive Decline Comparing a Sample of Community-Dwelling People Taking Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Over Time.

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Hypertension is an established risk factor for dementia. However, it is unclear whether there are differential effects of angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptor blockers (ARB) on brain health. In human observational studies, the evidence for superiority

Brain angiotensin and dopaminergic degeneration: relevance to Parkinson's disease.

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The pathogenic mechanism of Parkinson's disease (PD) appears to be multifactorial. However, oxidative stress and neuroinflammation, including activation of NADPH-dependent oxidases, play a major role in the progression of dopaminergic cell death. The renin-angiotensin system (RAS) was described as a

Renin-Angiotensin System Blockage and Avoiding High Doses of Calcineurin Inhibitors Prevent Interstitial Fibrosis and Tubular Atrophy in Kidney Transplant Recipients.

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OBJECTIVE Chronic allograft dysfunction is a complex and multifactorial process characterized by progressive interstitial fibrosis and tubular atrophy. The finding of interstitial fibrosis and tubular atrophy is prevalent among kidney transplant patients receiving a calcineurin inhibitor-based

The angiotensin-(1-7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice.

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Angiotensin-(1-7) [Ang (1-7)] is a peptide belonging to the non-classical renin-angiotensin system (RAS). Ang (1-7), through its receptor Mas, has an opposite action to angiotensin II (Ang II), the typical peptide of the classical RAS axis. Ang II produces skeletal muscle atrophy, a pathological

Renin-Angiotensin System Inhibitor Usage and Age-Related Macular Degeneration among Hypertensive Patients: Results from the National Health and Nutrition Examination Survey, 2005-2008

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Purpose: To assess whether renin-angiotensin system inhibitor (RASI) utilization is associated with age-related macular degeneration (AMD) prevalence among hypertensive patients. Methods:

Valsartan ameliorates ageing-induced aorta degeneration via angiotensin II type 1 receptor-mediated ERK activity.

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Angiotensin II (Ang II) plays important roles in ageing-related disorders through its type 1 receptor (AT1 R). However, the role and underlying mechanisms of AT1R in ageing-related vascular degeneration are not well understood. In this study, 40 ageing rats were randomly divided into two groups:

Angiotensin-(1-7) Receptor Mas Deficiency Does Not Exacerbate Cardiac Atrophy Following High-Level Spinal Cord Injury in Mice.

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Experimental spinal cord injury (SCI) causes a morphological and functional deterioration of the heart, in which the renin-angiotensin system (RAS) might play a role. The recently discovered non-canonical axis of RAS with angiotensin-(1-7) and its receptor Mas, which is associated with

Blockers of Angiotensin Other Than Olmesartan in Patients With Villous Atrophy: A Nationwide Case-Control Study.

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OBJECTIVE To examine the association between the previous use of nonolmesartan angiotensin receptor blockers (ARBs) or any angiotensin-converting enzyme inhibitor (ACEI) and subsequent villous atrophy (VA) in patients with small-intestinal VA as compared with general population-matched

Testicular atrophy, zinc concentration, and angiotensin-converting enzyme activity in the testes of vitamin A-deficient rats.

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Angiotensin-converting enzyme (ACE) as a part of the renin angiotensin system (RES) regulates blood pressure and fluid and electrolyte homeostasis, and the enzyme is considered to have a function in reproduction. Reduced enzyme activities have been observed in atrophied testes as a results of zinc

L-threo-3,4-dihydroxyphenylserine enhances the orthostatic responses of plasma renin activity and angiotensin II in multiple system atrophy.

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We evaluated the effect of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) on the response of blood pressure and vasoactive factors during head-up tilt in patients with multiple system atrophy (MSA). After the daily oral administration of 300 mg L-threo-DOPS for 2 weeks we observed a significant

Angiotensin-converting enzyme in cerebrospinal fluid and risk of brain atrophy.

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BACKGROUND Higher angiotensin-converting enzyme (ACE) activity might increase the risk of Alzheimer's disease by increasing blood pressure, and subsequent development of cerebral small vessel disease (CSVD). Yet, it may also decrease this risk, as it functions to degrade amyloid-β, thereby reducing

Renal interstitial hydrostatic pressure and urinary sodium excretion in rats with angiotensin-converting enzyme inhibitor-induced papillary atrophy.

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The importance of angiotensin type-1 (AT1) receptor stimulation during renal development has recently been established in both pharmacological and knockout models. We have previously reported irreversible and progressive papillary atrophy and a reduced baseline renal interstitial hydrostatic

The relationship between angiotensin converting enzyme insertion/deletion polymorphism and age-related macular degeneration.

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BACKGROUND To assess the role of serum angiotensin converting enzyme (ACE) levels and ACE insertion /deletion (I/D) genetic polymorphism in Turkish age-related macular degeneration (AMD) patients and control subjects. METHODS This prospective study consisted of 78 patients with AMD and 68 control

Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

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Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system,

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