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Essential hypertension is a multifactorial condition affecting a large percentage of the adult Turkish population (33.7%). It induces Left ventricular hypertrophy (LVH) and dilatation, which can lead to heart failure. The reasons for the development of LVH in patients with essential hypertension have not been established, and whether or not LVH results from long-term blood pressure (BP) elevation or non-hemodynamic factors affecting the myocardium is still a matter of debate. The purpose of the present study was to determine the relationship between calcium metabolism and hypertension by comparing healthy individuals and patients newly diagnosed with mild and moderate essential hypertension, and to elucidate the role of non-hemodynamic factors in the development of LVH in the hypertensive group.
Twenty-seven patients with essential hypertension and 20 healthy individuals were compared with respect to calciotropic hormones, left ventricular mass index (LVMI), and urinary and serum biochemical parameters (Table 1) (Table 2). The correlations between parathormone, vitamin D, and calcitonin levels and LVMI and blood pressure elevation were determined. Written informed consent was obtained from each subject following a detailed explanation of the objectives and protocol of the study which was conducted in accordance with the ethical principles stated in the “Declaration of Helsinki” and approved by the institutional ethics committee. The data were analyzed using the Statistical Program for the Social Sciences (version 10.0; SPSS, Inc., Chicago, IL, USA).
The parathormone level was significantly higher (p=0.006) and vitamin D level was significantly lower (p=0.01) in the patient group compared with the control group. However, the two groups were similar in terms of albumin-corrected calcium levels, which were within the normal range (p=0.988). The serum sodium (p=0.014) and urinary calcium (p=0.003) levels and LVMI (p<0.01) were also significantly higher in the patient group. No significant correlations were determined between ambulatory blood pressure and parathormone and vitamin D levels, but a significant correlation was found between LVMI and parathormone level (p=0.06) in hypertensive patients.
We suggest that essential hypertension alters calcium metabolism. Specifically, calciuresis develops secondary to hypertabolism. Specifically, calciuresis develops secondary to hypernatremia, with a compensatory release of PTH. Meanwhile, the increased levels of PTH cause a rise in general protein synthesis, which leads to the development of myocardial hypertrophy. However, since the small sample size in the present study precludes our ability to draw precise conclusions, an in-depth analysis of the relationship between PTH, vitamin D, and blood pressure, via future large-scale studies, is warranted.
|Patient group n:27, Mean ±SD||Control group n:20, Mean ±SD||p value|
|Vitamin D (ng/mL)||11.03±1.57||17.38±7.21||0.010|
viding LVM by body surface area. Na: sodium, K: potassium, Ca: calcium, P: phosphorus, ALP: alkaline phospha- tase, PTH: parathormone, SD: standard deviation
|Patient group n:27 Mean±SD||Patient group n:20 Mean±SD||p value|
|Urinary Ca (mg/24 h)||275.56±82.09||203.50±72.00||0.003|
|Urinary P (g/24 h)||0.86±0.24||0.92±0.23||0.409|
OH-proline (mmol/mol c
|Urinary creatinine (g/24 h)||1.31±0.39||1.42±0.39||0.349|
Ca: calcium, P: phosphorus, OH-proline: hydroxyproline, SD: standard deviation, c:creatinin