Candesartan Cilexetil Improves Left Ventricular Function, Left Ventricular Hypertrophy, and Endothelial Function in Patients With Hypertensive Heart Disease.

Isobe, Naoki; Taniguchi, Koichi; Ono, Zenpei; Adachi, Hitoshi; Toyama, Takuji; Naito, Shigeto; Hara, Hiroshi; Kono, Hiroshi

doi:10.1253/circj.66.993

Cited by 25 publications

(24 citation statements)

References 42 publications

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“…7 An acute functional change in vascular smooth muscle relaxation, improvement in endothelial dysfunction, decrease in arterial wall thickness, decrease in collagen content and reversal of smooth muscle cell hypertrophy have been proposed as mechanisms of the improvement in PWV by ARB. [21][22][23] However, it is unlikely that treatment with ARB for only 4 weeks would improve the structure of the vasculature. Short-term treatment of ARB may improve PWV mainly through functional mechanisms such as vascular smooth muscle relaxation and improvement in endothelial dysfunction, because BP was also decreased after ARB treatment.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Receptor Blocker Prevents Increased Arterial Stiffness in Patients With Essential Hypertension

Agata

Nagahara

Kinoshita

et al. 2004

Circ J

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ulse wave velocity (PWV) reflects arterial distensibility, and aortic PWV in particular is associated with major cardiovascular risk factors and is a strong predictor of prognosis in patients with hypertension. 1,2 Aortic PWV, measured from the carotid to femoral arteries, evaluates aortic stiffness, but its measurement requires complex techniques and has not shown reproducibility. Recently, a simple, noninvasive and automatic method of measuring brachial -ankle PWV (baPWV) has been developed, and the validity and reproducibility of this new technique have been demonstrated. 3 As it has been reported that the baPWV value has positive correlations with PWV, measured by the classical method, carotid intima -media thickness (IMT) and abdominal aortic calcification, 4-6 this new method might enable prediction of the risk of atherosclerosis. Currently, angiotensin II receptor blockers (ARB) are widely used for the treatment of HT because they have been reported to reduce both arterial stiffness and blood pressure (BP). 7 However, BP is one of the main factors affecting arterial stiffness, and the direct effect of ARB on arterial stiffness excluding the effect of BP has not been elucidated Adiponectin, an adipocyte-derived protein referred to as Acrp30, apM1, AdipoQ or GBP28, has been identified and characterized, [8][9][10][11][12] and in contrast to other adipocyte-derived proteins such as tumor necrosis factor (TNF-), plasminogen activator inhibitor-1, leptin and resistin, the circulating concentrations of adiponectin are reduced in patients with coronary artery disease and in states of insulin resistance such as obesity and type 2 diabetes. [13][14][15] It has been suggested that adiponectin enhances insulin sensitivity and prevents atherosclerosis. 16,17 We recently reported that treatment with an ARB for a period of 2 weeks not only improved insulin resistance but also increased adiponectin concentrations in subjects with essential hypertension (EHT). 18 The present study was design to test our hypotheses that this improvement of insulin resistance and increase in adiponectin after treatment with an ARB may prevent progression of atherosclerosis or arterial stiffness. One of the aims was to elucidate the long-term effect of ARB on arterial stiffness excluding it effect on BP, and the other was to evaluate the role of adiponectin in the chronic effect of ARB. Methods Study Protocol 1Nine subjects with EHT who had not been taking anti-hypertensive drugs or who had been taking anti-hypertensive drugs other than ARB or angiotensin-converting enzyme inhibitor (ACEI) but whose BP remained high were enrolled. After measurement of baPWV and BP as described later, the subjects were treated with an ARB (80 mg valsartan, Background High pulse wave velocity (PWV) is related to cardiovascular risk in essential hypertension (EHT). It is reported that short-term treatment with an angiotensin II receptor blocker (ARB) decreases PWV, as well as blood pressure (BP), and increases the serum adiponectin, known as an adipocytokine, ...

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Section: Discussionmentioning

confidence: 99%

Angiotensin II Receptor Blocker Prevents Increased Arterial Stiffness in Patients With Essential Hypertension

Agata

Nagahara

Kinoshita

et al. 2004

Circ J

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“…ACEI and ARB are reportedly hypotensive agents that have a preventive effect on myocardial remodeling, anti-inflammatory actions and improve that function of the vascular endothelial cells. 26,27 However, these actions have not yet been fully elucidated. Therefore, we evaluated the changes in the renin -angiotensin system that were antagonistic to ANP by treating rats with drugs that block the reninangiotensin system in order to elucidate the relationship between ANP and the renin -angiotensin system in NO inhibitor-induced hypertension.…”

Section: Discussionmentioning

confidence: 99%

Effectiveness of Angiotensin-Converting Enzyme Inhibitor or Angiotensin II Receptor Blocker on Atrial Natriuretic Peptide

Sata

Tanaka

Suzuki

et al. 2003

Circ J

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umerous vasoactive substances are involved in the regulation of blood pressure, including reninangiotensin, atrial natriuretic peptide (ANP), endothelium-derived relaxing factor (EDRF), endothelin, and adrenomedullin. In 1986, it was established that EDRF is nitric oxide (NO), 1 which is secreted by vascular endothelial cells and maintains the homeostasis of vascular walls. The main effects of endothelim-derived NO in the circulatory system are relaxation of vascular smooth muscle and regulation of blood pressure. ANP was first isolated and characterized in 1984. 2 It is primarily synthesized and stored as granules in the cardiac atrium, and rapidly released into the blood stream during increased atrium Circulation Journal Vol.67, December 2003 load. The major effects of ANP are lowering of blood pressure, and water and sodium diuresis; and thus it is an important hormone in blood pressure regulation. The renin -angiotensin system also plays an important role in regulating blood pressure. Both angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blocker (ARB) are hypotensive agents that are involved in this system, and these agents are most useful drugs in the clinical setting because they have cardioprotective actions.Previous studies have reported on the administration of NO inhibitors, which increase blood pressure, and have dealt with the administration of ACEI and ARB. However, there is little information on the evaluation of ANP mRNA expression, ANP granules, ANP immunostaining, and changes in plasma ANP concentrations. Therefore, the present study examined the relationship between NO and ANP as vasoactive substances. Methods NO Inhibitor TreatmentNormotensive rats (Jcl: Wistar males, 30-40 g, 3 weeks old) were purchased from CLEA Japan (Kagoshima, Japan). Treatment was started at age 4 weeks and continued for 8 weeks. NO inhibitor was mixed into the food, and The aim of this study was to evaluate the effectiveness of an angiotensin-converting enzyne inhibitor (ACEI, quinapril) or angiotensin II receptor blocker (ARB, candesartan) on atrial natriuretic peptide (ANP) activity in rats with hypertension induced by nitric oxide (NO) inhibition. ACEI and ARB have a number of pharmacologic effects, including blood pressure reduction, myocardial preservation, and an unknown effect in the circulation. The changes in ANP in NO inhibitor-induced hypertensive rats were evaluated in order to elucidate the interaction between ANP and NO in the regulation of blood pressure. Thirty-six rats were divided into 4 groups and administered the experimental agents for 8 weeks: group Control was given regular food (n=9), group N G -nitro-L-arginine (L-NNA) was administered L-NNA (25mg·kg -1 ·day -1 , n=9), group ACEI was administered L-NNA and quinapril (10 mg·kg -1 ·day -1 , n=9), and group ARB was administered L-NNA and candesartan (10mg·kg -1 · day -1 , n=9 2) increased significantly. NO inhibitorinduced hypertension caused no changes in ANP concentrations. However, the ACEI and ARB had a direct effe...

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“…5,6 Previous studies have shown LVH to be related to an impaired EDV in hypertensive subjects. [7][8][9][10][11][12][13][14] However, the relationship between EDV and LVMI has not been investigated in a general population. Furthermore, as the degree of EDV in peripheral conductance arteries and resistance arteries are not closely related, [15][16][17] there is a need to clarify the relationship between EDV in these two types of arteries and LVMI in the same individuals.…”

Section: Introductionmentioning

confidence: 99%

Left ventricular mass is related to endothelium-dependent vasodilation in the forearm, but not in the brachial artery, in elderly subjects: the Prospective Investigation of the Vasculature in Uppsala Seniors study

Lind

2008

J Hum Hypertens

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Left ventricular hypertrophy (LVH) is a powerful cardiovascular risk factor and has previously been related to endothelium-dependent vasodilation (EDV) in hypertensive patients. In the Prospective Investigation of the Vasculature in Uppsala Seniors study, different techniques to evaluate EDV in different types of vessels were applied and were related to left ventricular mass index (LVMI) in the general population. In 1016 subjects aged 70 years, EDV was evaluated by the invasive forearm technique with acetylcholine given in the brachial artery, the brachial artery ultrasound technique with measurement of flow-mediated dilatation (FMD) and the pulse wave analysis method with b-2-agonist (terbutaline) provocation. LVMI was determined by echocardiography. LVMI was related to both EDV and the pulse wave-based technique (both r ¼ À0.14, Po0.0001) in univariate analysis. LVMI was also weakly related to FMD (r ¼ À0.07, P ¼ 0.046). However, in multiple regression analysis adjusted for gender, systolic and diastolic blood pressure and use of antihypertensive medication, only EDV was associated with LVMI (P ¼ 0.016). EDV was mainly reduced in those with left ventricular concentric hypertrophy (P ¼ 0.0012). In conclusion, in a population-based sample of elderly subjects, EDV, but not FMD, was inversely correlated with LVM independent of blood pressure, suggesting that EDV in resistance arteries is of more importance for LVH than endothelial vasodilatory function in conduit arteries in the elderly.

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Candesartan Cilexetil Improves Left Ventricular Function, Left Ventricular Hypertrophy, and Endothelial Function in Patients With Hypertensive Heart Disease.

Cited by 25 publications

References 42 publications

Angiotensin II Receptor Blocker Prevents Increased Arterial Stiffness in Patients With Essential Hypertension

Angiotensin II Receptor Blocker Prevents Increased Arterial Stiffness in Patients With Essential Hypertension

Effectiveness of Angiotensin-Converting Enzyme Inhibitor or Angiotensin II Receptor Blocker on Atrial Natriuretic Peptide

Left ventricular mass is related to endothelium-dependent vasodilation in the forearm, but not in the brachial artery, in elderly subjects: the Prospective Investigation of the Vasculature in Uppsala Seniors study

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