Vascular and metabolic effects of angiotensin II receptor blockers

Barra, Silvia; Vitagliano, Alice; Cuomo, Vittoria; Vitagliano, Giancarlo; Gaeta, Giovanni Battista

doi:10.1517/14656560802653180

Cited by 18 publications

(14 citation statements)

References 92 publications

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“…Medications use for reduce activity of reninangiotensin system is probably the only one tool in the treatment of these patients. Angiotensin receptor type I blockers have several advantages, that confi rmed by the literature data [4,9]. Our study revealed regression of LVH and its signifi cant decrease.…”

Section: Methodssupporting

confidence: 84%

Arterial hypertension, cardiovascular remodeling and plasma level of osteopontin in patients with end-stage kidney disease on hemodialysis

Візір¹,

Ovska²,

Sadomov³

2014

ZMJ

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Large population-based studies acknowledge that patients with chronic kidney disease (CKD) have high risk of cardiovascular (CV) diseases regardless of etiology, especially in its late stages. Deceleration of glomerular fi ltration on every 10 mL/min increases cardiovascular risk and risk of death from any causes up to 20 %, that reaches the maximum level in patients on renal replacement therapy [2,11]. Lesion of cardiovascular system in subjects suffering from CKD occurs in different pathogenic mechanisms simultaneously. One of the main factors of development the CV remodeling in dialysis patients is arterial hypertension (AH). It occurs as a result of volume overload, anemia and existing arteriovenous fi stula [3]. Further the number of investigators pay a special attention to bone mineral violations in the development of the CV remodeling, specifi cally to high level of phosphate and vascular calcifi cation (VC) [5,18]. The extracellular phosphate mechanism of action is induction of the osteoblastic differentiation factors. One of this factors is osteopontin (OP) [10]. As pleotropic cytokine this major noncollagenous bone matrix protein is expressed in mineralized tissue and synthesized by fi broblasts, osteoblasts, smooth muscle and endothelial cells [6,23]. OP regulation is not completely investigated yet. But there are results of the protein activity stimulation due to activity of proinfl ammatory cytokines, angiotensin II [12]. Literature data indicate the expression of OP in hypertrophied myocardium [1]. This cytokine is believed to cause smooth muscle cells proliferation and elastic membrane degradation, thus to trigger processes of vascular remodeling. The negative role of OP in the development of diastolic dysfunction in patients Aim. Large population-based studies acknowledge that patients with chronic kidney disease have a high risk of cardiovascular diseases regardless of etiology, especially in its late stages. The aim of this study was to investigate the features of arterial hypertension, cardiovascular remodeling and plasma level of osteopontin in dynamics of candesartan therapy, as well as to identify the relationships between studied parameters in patients with chronic kidney disease treated by hemodialysis.Methods and results. 50 patients were performed ambulatory blood pressure monitoring, the plasma level of osteopontin was determined by ELISA method, standard echocardiography and ultrasonography of common carotid after treatment of candesartan during 12 weeks.Conclusion. The results indicate that the use of candesartan cilexetil in hemodialysis populations promotes regression of left ventricular hypertrophy and vascular remodeling indices, has antihypertensive effect.Артеріальна гіпертензія, кардіоваскулярне ремоделювання та плазмовий рівень остеопонтину в пацієнтів із кінцевою стадією хронічної хвороби нирок на гемодіалізі В. А. Візір, О. Г. Овська, А.С. СадомовМасштабні популяційні дослідження свідчать, що пацієнти з термінальною нирковою недостатністю мають високий ризик розвитку серцев...

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Section: Methodssupporting

confidence: 84%

Arterial hypertension, cardiovascular remodeling and plasma level of osteopontin in patients with end-stage kidney disease on hemodialysis

Візір¹,

Ovska²,

Sadomov³

2014

ZMJ

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“…RAS blockers reduce proteinuria by acting on intraglomerular pressure, mesangial contractility and proximal tubular solute transport [27]. Moreover, RAS blockers improve the endothelial function, inflammation, IR and oxidative stress [28,29]. RAS blockers also increase plasma adiponectin levels while decreasing proteinuria in patients with DN [30].…”

Section: Discussionmentioning

confidence: 99%

Effect of Irbesartan on Chemerin in the Renal Tissues of Diabetic Rats

Yu¹,

Zhang²,

Xu³

et al. 2015

Kidney Blood Press Res

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Background/Aims: Chemerin was introduced as a novel adipokine that plays a crucial role in insulin signaling and diabetic nephropathy. Serum chemerin levels are significantly elevated in type 2 diabetes patients with macroalbuminuria. However, the underlying mechanisms remain unclear. We conducted a preliminary investigation of the effects of the renin-angiotensin system (RAS) on chemerin expression in streptozotocin-induced diabetic rats. Methods: Streptozotocin-induced diabetic rats were randomized into control, diabetic, and irbesartan-treated groups. Real-time polymerase chain reaction was used to detect mRNA expression of chemerin, angiotensin II type 1a receptor (AT1a), angiotensin II type 1b receptor (AT1b) and angiotensin II type 2 receptor (AT2). Immunohistochemical staining was used to detect chemerin in renal tissues. Results: Expression levels of chemerin in renal tissues were significantly elevated in the diabetic group compared to the control group. In the irbesartan-treated group, chemerin expression levels and RAS-related protein levels (i.e. AT1a and AT1b) were markedly decreased compared to the diabetic group. Irbesartan treatment reduced chemerin overexpression and RAS-related protein levels in diabetic rats (i.e. AT1a and AT1b). Conclusion: Irbesartan may inhibit intrarenal RAS in diabetic rats, which may affect the expression of chemerin in the kidneys; however, the precise underlying mechanism remains to be determined.

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“…ACE inhibitors prevent the de novo synthesis of angiotensin II, while ARB's block interaction between angiotensin II and its receptor. Many studies have demonstrated that the therapeutic actions of both ACE-I and ARBs, particularly the latter, extend beyond blood pressure reduction (11, 12). The wide-ranging effects of the RAS are due in part to the systemic and local paracrine and autocrine functions of the RAS within individual organs, such as the brain (13) or kidney (14) .…”

Section: Introductionmentioning

confidence: 99%

The Renin-Angiotensin Pathway in Posttraumatic Stress Disorder

Khoury¹,

Marvar²,

Gillespie³

et al. 2012

J. Clin. Psychiatry

121

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Objective PTSD is a debilitating stress-related illness associated with trauma exposure. The peripheral and central mechanisms mediating stress response in PTSD are incompletely understood. Recent data suggest that the renin-angiotensin pathway, essential to cardiovascular regulation, is also involved in mediating stress and anxiety. In this study, the authors examined the relationship between active treatment with blood pressure medication, including angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs), and PTSD symptom severity within a highly traumatized civilian medical population. Method Cross-sectional, observational data was analyzed from a larger study, recruiting patients from Grady Memorial Hospital's outpatient population from 2006 to November 2010. Multi-variable linear regression models were fit to statistically evaluate the independent association of being prescribed an ACE-I or ARB with PTSD symptoms, using a sub-set of patients for whom medical information was available (n=505). PTSD diagnosis was assessed using the modified PTSD Symptom Scale (PSS) based on DSM-IV criteria with PTSD symptoms based on PSS and Clinician Administered PTSD Scale (CAPS). Results A significant association was determined between presence of ACE-I / ARB medication and decreased PTSD symptoms (mean PSS score 11.4 vs 14.9 for individuals prescribed vs not prescribed ACE-I/ARBs, respectively (p = 0.014)). After adjustment for covariates, ACE-I/ARB treatment remained significantly associated with decreased PTSD symptoms (p = 0.044). Notably, other blood pressure medications, including beta-blockers, calcium channel blockers, and diuretics, were not significantly associated with reduced PTSD symptoms. Conclusions These data provide the first clinical evidence supporting a role for the reninangiotensin system in the regulation of stress response in patients diagnosed with PTSD. Further studies should examine whether available medications targeting this pathway should be considered for future treatment and potential protection against PTSD symptoms.

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Vascular and metabolic effects of angiotensin II receptor blockers

Cited by 18 publications

References 92 publications

Arterial hypertension, cardiovascular remodeling and plasma level of osteopontin in patients with end-stage kidney disease on hemodialysis

Arterial hypertension, cardiovascular remodeling and plasma level of osteopontin in patients with end-stage kidney disease on hemodialysis

Effect of Irbesartan on Chemerin in the Renal Tissues of Diabetic Rats

The Renin-Angiotensin Pathway in Posttraumatic Stress Disorder

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