Influence of dietary sodium on the renin–angiotensin–aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria

Abstract

We investigated the interplay of dietary sodium and renin-angiotensin-aldosterone system (RAAS) activity with the prevalence of left ventricular hypertrophy (LVH) in essential hypertension. Electrocardiograms (EKG) were reviewed for the presence of LVH in 160 hypertensive patients. We then compared the rate of LVH to levels of plasma renin activity (PRA) and serum aldosterone under high and low sodium diet conditions. On high sodium diet, serum aldosterone was significantly higher (7.770.93 vs 5.770.35 ng/dl, P ¼ 0.02) in participants with LVH. With low sodium diet and upright posture, PRA was significantly lower in subjects with LVH vs those without (5.671.1 vs 7.670.56 ng/ml/h, P ¼ 0.026). Aldosterone levels on low sodium diet were not different between those with and those without LVH. PRA was then dichotomized at the lowest quartile under low sodium/upright posture conditions to define a 'low renin' group. In a multivariate logistic regression containing renin status (low renin vs normal/high renin), aldosterone on a high sodium diet, age, body mass index, gender, race, duration of hypertension, systolic and diastolic blood pressure and salt-sensitivity only low-renin status on a low sodium diet (P ¼ 0.019) and serum aldosterone on a high sodium diet (P ¼ 0.04) were significant predictors of LVH. Thus, reduced modulation of renin activity in response to sodium restriction and an increased aldosterone on a high sodium diet appear to identify characteristics of hypertensive patients predisposed to abnormal cardiac remodelling.

Nonmodulation as the Mechanism for Salt Sensitivity of Blood Pressure in Individuals with Hypertension and Type 2 Diabetes Mellitus

“…Details of this protocol have been described previously (4,24,25). In brief, to control for the influence of medications on components of the RAAS, all angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers, or mineralocorticoid receptor antagonists were discontinued for 3 months and ␤-blockers and diuretics were discontinued for 1 month before the study.…”

“…alt sensitivity of blood pressure occurs frequently in individuals with type 2 diabetes mellitus (T2DM) and is associated with an increased risk for left ventricular hypertrophy (LVH), renal disease, and cardiovascular death (1)(2)(3)(4). The underlying cause of salt sensitivity in individuals with T2DM is unknown.…”

“…The first, the LR phenotype, displays a diminished rise in plasma renin activity (PRA) in the setting of low sodium balance (4). The second, nonmodulation (NMOD), exists within individuals that are capable of mounting a normal physiological renin response to low sodium balance but display a blunted adrenal aldosterone secretion in response to exogenous angiotensin II (ANGII) stimulus (16 -18).…”

Adrenal function in 23 children with paracoccidioidomycosis

“…These data were not compatible with mineralocorticoid insufficiency, and it can be explained by hypoalbuminemia, which is common in these PCM patients 18 , or different level of dietary sodium 22 , which was not controlled in this study. The relationship between hypoalbuminemia and cases with more severity and/or more time of disease was also not established in these cases.…”

Cardiac changes in pediatric liver transplant recipients: are they truly irreversible?

“…Angiotensin II also improves coronary artery permeability, thereby permitting growth factors to diffuse into the myocardium [12]. Excess sodium independent of volume overload can also lead to cardiac hypertrophy, and this appears to be mediated by excess aldosterone [13] as the use of an aldosterone antagonist can ameliorate the cardiac hypertrophy [14]. All of these will increase cardiac stiffness and promote diastolic dysfunction.…”