Microalbuminuria, left ventricular mass and ambulatory blood pressure in essential hypertension.

Redón, Josep; Baldó, Emilio; Bertolín,; Lozano, JV; Miralles, Amparo; Jm, Pascual

doi:10.1016/0895-7061(95)97679-l

Cited by 18 publications

(20 citation statements)

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“…Even though UACR and LV mass assessed by ECG were related to systolic BP, the association between them existed independently of systolic BP at baseline and after 1 year of antihypertensive treatment, as well as independently of changes in systolic BP during treatment. These BP independent relationship support previous findings 23,24 and suggest either a BP independent pathogenetic or genetic relationship between cardiac and glomerular vascular damage in hypertension.…”

Section: Discussionsupporting

confidence: 90%

“…These patients might also be more prone to regression of cardiovascular changes following BP reduction during antihypertensive treatment. The association between elevated urine albumin excretion and cardiovascular hypertrophy in essential hypertension demonstrated by us 15 and others 23,24,[26][27][28][29] may, therefore, be due not only to higher BP in these patients but also a generalised increased cardiovascular sensibility to BP-induced cardiovascular changes. Therefore, we plan to investigate whether these patients have special genetic polymorphisms within the renin-angiotensin system 33 such as angiotensinconverting enzyme polymorphism (ACE*I/D), angiotensinogen polymorphism (AGT*T/C) and angiotensin II-receptor type 1 polymorphism (AT1R*A/C).…”

Section: Journal Of Human Hypertensionmentioning

confidence: 94%

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A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study

et al. 2002

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In the Losartan Intervention For Endpoint reduction (LIFE) study left ventricular (LV) hypertrophy was associated with increased urine albumin/creatinine ratio (UACR) at baseline. To evaluate whether this association was due only to parallel blood pressure (BP)-induced changes we re-examined the patients after 1 year of antihypertensive treatment to investigate whether changes in LV hypertrophy and UACR were related independently of changes in BP. In 7142 hypertensive patients included in the LIFE study, we measured UACR, LV hypertrophy by electrocardiography, plasma glucose and BP after 2 weeks of placebo treatment and again after 1 year of antihypertensive treatment with either an atenolol or a losartan based regime. At baseline and still after 1 year of treatment logUACR (R = 0.28, P Ͻ 0.001) was still correlated to LV hypertrophy (␤ = 0.05) assessed by ECG independently of systolic BP (␤ = 0.16), plasma glucose (␤ = 0.19) and age (␤

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Section: Discussionsupporting

confidence: 90%

Section: Journal Of Human Hypertensionmentioning

confidence: 94%

A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study

et al. 2002

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“…25 Microalbuminuria has been related to other "surrogate markers" of high cardiovascular risk such as left ventricular hypertrophy, independent of BP. 26 The reductions in microalbuminuria seen in this study are therefore consistent with the reductions in left ventricular mass index seen in various studies of indapamide SR and enalapril. However, in the 1-year left ventricular hypertrophy regression, indapamide versus enalapril (LIVE) study, indapamide SR was found to be significantly more effective than enalapril at reducing left ventricular mass index.…”

Section: Discussionsupporting

confidence: 77%

Efficacy of Indapamide SR Compared With Enalapril in Elderly Hypertensive Patients With Type 2 Diabetes

Puig

Marre

Kokot³

et al. 2007

American Journal of Hypertension

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Background: Blood pressure control is the main influential variable in reducing microalbuminuria in patients with type 2 diabetes. In this subanalysis of the Natrilix SR versus Enalapril Study in hypertensive Type 2 diabetics with micrOalbuminuRia (NESTOR) study, we have compared the effectiveness of indapamide sustained release (SR) and enalapril in reducing blood pressure and microalbuminuria in patients ≥65 years of age.

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“…Creatinine clearance at the end of experiments was calculated. Urinary excretion of albumin was determined by the immunonephelemetric method (33).…”

Section: Methodsmentioning

confidence: 99%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Rugale, Caroline, Sandrine Delbosc, Jean-Paul Cristol, Albert Mimran, and Bernard Jover. Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension. Am J Physiol Heart Circ Physiol 284: H1744-H1750, 2003. First published December 5, 2002 10.1152/ajpheart.00864.2002The influence of a low-sodium (LS) diet was assessed on the cardiac and renal alterations and pro-oxidant effect associated with a 10-day infusion of angiotensin II (200 or 400 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 , osmotic pumps). Tail-cuff pressure (TCP), albuminuria, and renal blood flow were determined at the end of the experiments. Heart weight index (HWI) and production of superoxide anion (O 2 Ϫ ⅐) by the left ventricle and H2O2 by the aorta was measured with the use of bioluminescence. Although the final TCP was similar in LS and normal sodium (NS) rats infused with high and low doses of angiotensin II, respectively, the increase in HWI was prevented by the LS diet. Sodium restriction reduced the rise in albuminuria without a change in the renal effect of angiotensin II. The increased production of O 2 Ϫ ⅐ and H2O2 observed in NS rats was abrogated in LS rats. The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide. heart weight; albuminuria; reactive oxygen species; renal hemodynamic THE DEVELOPMENT OF cardiac hypertrophy results from the interaction between several factors, including elevated arterial pressure, angiotensin II (ANG II), and sodium intake. Although blood pressure is an important determinant of cardiac mass (8), ANG II may directly increase protein synthesis and cause myocyte hypertrophy, as reported in cultured cardiac myocytes isolated from chicks (2) and neonatal rats (34). In vivo long-term administration of an initially subpressor dose of ANG II, a model that mimics the development of human hypertension, induces a gradual rise in blood pressure associated with a cardiac hypertrophy (7,14,17). However, ANG II might increase cardiac mass independently of arterial pressure. This was suggested by the presence of cardiac hypertrophy in rats infused with a nonpressor dose of the peptide (4, 37) or in rats infused with a pressor dose of ANG II and concomitantly treated by hydralazine (7, 37).The concentration of sodium ion in vitro or dietary sodium intake in vivo may modulate cardiac mass. In cultured neonatal rat myocardial myoblasts, cellular protein content and cell size increased when sodium concentration of the medium was augmented (15). In vivo, a high-sodium intake increased cardiac mass in normotensive rats (46) and exacerbated cardiac hypertrophy in hypertensive rats (12). In humans, sodium intake (assessed by urinary sodium excretion) and the left ventricular mass index were positively correlated in hypertensive and normotensive subjects (9). Conversely, a low-sodium (LS) intake prevents cardiac hypertrophy associated with two-k...

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Microalbuminuria, left ventricular mass and ambulatory blood pressure in essential hypertension.

Cited by 18 publications

References 0 publications

A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study

A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study

Efficacy of Indapamide SR Compared With Enalapril in Elderly Hypertensive Patients With Type 2 Diabetes

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

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