Relations of Serum Aldosterone to Cardiac Structure

Vasan, Ramachandran S.; Evans, Jane C.; Benjamin, Emelia J.; Levy, Daniel; Larson, Martin G.; Sundström, Johan; Murabito, Joanne M.; Sam, Flora; Colucci, Wilson S.; Wilson, Peter W.F.

doi:10.1161/01.hyp.0000124251.06056.8e

Cited by 123 publications

(60 citation statements)

References 46 publications

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“…[24][25][26] It has been suggested that hypertensive incidents and organ damage in humans may occur even at plasma aldosterone levels within the normal physiological range. 24,[27][28][29] Therefore, targeting aldosterone synthesis and release may be clinically important in preventing cardiovascular disease. Ca 2+ ions are conveyed through the T-type Ca channel to the mitochondria, where they activate aldosterone synthesis, which in turn stimulates T-type Ca channel expression, 30,31 creating a positive feedback loop of aldosterone biosynthesis in adrenal cells.…”

Section: Discussionmentioning

confidence: 99%

Benidipine reduces albuminuria and plasma aldosterone in mild-to-moderate stage chronic kidney disease with albuminuria

et al. 2010

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Benidipine inhibits both L-and T-type Ca channels, and has been shown to dilate the efferent arterioles as effectively as the afferent arterioles. In this study, we conducted an open-label and randomized trial to compare the effects of benidipine with those of amlodipine on blood pressure (BP), albuminuria and aldosterone concentration in hypertensive patients with mild-tomoderate stage chronic kidney disease (CKD). Patients with BPX130/80 mm Hg, with estimated glomerular filtration rate (eGFR) of 30-90 ml min À1 per 1.73 m 2 , and with albuminuria430 mg per g creatinine (Cr), despite treatment with the maximum recommended dose of angiotensin II receptor blockers (ARBs) were randomly assigned to two groups. Patients received either of the following two treatment regimens: 2 mg per day benidipine, which was increased up to a dose of 8 mg per day (n¼52), or 2.5 mg per day amlodipine, which was increased up to a dose of 10 mg per day (n¼52). After 6 months of treatment, a significant and comparable reduction in the systolic and diastolic BP was observed in both groups. The decrease in the urinary albumin to Cr ratio in the benidipine group was significantly lower than that in the amlodipine group. Although plasma renin activity was not different in the two groups, plasma aldosterone levels were significantly decreased in the benidipine group. Moreover, urinary Na/K ratio was significantly decreased in the benidipine group but remained unchanged in the serum. It may be concluded that benidipine results in a greater reduction of plasma aldosterone and albuminuria than amlodipine, and that these effects are independent of BP reduction.

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Section: Discussionmentioning

confidence: 99%

Benidipine reduces albuminuria and plasma aldosterone in mild-to-moderate stage chronic kidney disease with albuminuria

et al. 2010

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“…Accordingly, it could be speculated that the presumably low levels of endogenous estradiol in our female and the presumably low levels of testosterone in our mainly elderly male study population may be partly responsible for the observed higher susceptibility of female hearts for hypertrophic stimuli, i.e., adiposity. Additional explanatory effects could be interactions between the signaling effects of estrogen and aldosterone receptors (39,40); however, in the largest study, sex-related differences of serum aldosterone on left ventricular geometry were independent of menopausal status and BMI (41).…”

Section: Left Ventricular Mass In Diabetesmentioning

confidence: 90%

Sex-Specific Determinants of Left Ventricular Mass in Pre-Diabetic and Type 2 Diabetic Subjects

et al. 2007

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OBJECTIVE -Obesity and hypertension are regarded as the most important determinants of left ventricular mass in the community. Little is known about sex-specific influences of obesity, hypertension, and other risk factors on left ventricular mass in pre-diabetic or diabetic subjects.RESEARCH DESIGN AND METHODS -We examined how body composition, blood pressure, and other factors are related to left ventricular structure in elderly subjects (mean age 62 years, 88% of women postmenopausal) with pre-diabetes (impaired fasting glucose or impaired glucose tolerance; n ϭ 112) and diabetes with (n ϭ 181) and without (n ϭ 213) overt cardiovascular disease (CVD).RESULTS -Neither microalbuminuria nor physical activity was significantly associated with left ventricular mass. In pre-diabetic as well as diabetic subjects with CVD, mainly BMI and fat mass, particularly in women, were correlated with left ventricular mass. In the diabetic group without overt CVD, fat mass was only slightly correlated with left ventricular mass. In the latter group waist-to-hip-ratio, and, only in men, systolic blood pressure, glucose, and A1C were moderately correlated with left ventricular mass. Multiregression analysis over all groups again revealed fat mass as the main determinant of left ventricular mass in women. In women but not men obesity was associated with a significantly increased prevalence of concentric left ventricular hypertrophy.CONCLUSIONS -In pre-diabetic and diabetic elderly subjects fat mass is the major determinant of left ventricular mass in women but not in men. These results may partly explain sex differences in CVD mortality in obese elderly diabetic subjects and underscore the need for activities focused on weight reduction. Diabetes Care 30:946 -952, 2007L eft ventricular hypertrophy is independently associated with congestive heart failure and cardiovascular mortality (1-3). Diabetes is also known as an important risk factor for cardiovascular morbidity and mortality, and this association is partly mediated by its effect on left ventricular structure. Traditionally, hypertension and obesity have been regarded as the most important etiological factors in the development of left ventricular hypertrophy in the community (4 -8). Diabetes and impaired glucose tolerance (IGT) or impaired fasting glucose (IFG), the latter being regarded as a preclinical stage of diabetes, are also recognized as independent risk factors for the development of left ventricular hypertrophy (9 -11). However, the role of the traditional etiological risk factors in prediabetic or diabetic subjects is unknown. In patients with more advanced stages of diabetes, in particular, it has been speculated that the traditional risk factors for left ventricular hypertrophy may have a lesser influence on left ventricular mass because of other mechanisms that may become more important (12). Furthermore, although it is known that in the general population cardiac adaptations to obesity and hypertension are sex-specific (7,8) and, in addition, influences of di...

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“…The carotid IMT is thicker in men than in women across all ages (36). Age, systolic blood pressure, total cholesterol, HDL cholesterol, body mass index and smoking were independent predictors of IMT in both sexes (36 (19,20 …”

Section: Morimoto Et Al Assessed the Salt Sensitivity In About 350mentioning

confidence: 99%

“…It was reported that LVH has a greater impact on survival in women than in men both in the patients with and without coronary artery disease (16,17 (18)(19)(20)(21)(22)(23)(24). The two major factors in the pathogenesis of LVH postulated on the basis of experimental results are hemodynamic and non-hemodynamic factors (24).…”

Section: T a B L E 6 S T E P Wi S E Mu L T I P L E Re G R E S S I Omentioning

confidence: 99%

Gender-related Differences in Target Organ Damage in Untreated Patients with Essential Hypertension

et al. 2006

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Relations of Serum Aldosterone to Cardiac Structure

Cited by 123 publications

References 46 publications

Benidipine reduces albuminuria and plasma aldosterone in mild-to-moderate stage chronic kidney disease with albuminuria

Benidipine reduces albuminuria and plasma aldosterone in mild-to-moderate stage chronic kidney disease with albuminuria

Sex-Specific Determinants of Left Ventricular Mass in Pre-Diabetic and Type 2 Diabetic Subjects

Gender-related Differences in Target Organ Damage in Untreated Patients with Essential Hypertension

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