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• W2544512911 abstract "It has been known that salt-sensitivity of blood pressure is defined genetically as well as can be developed secondary to either decreased renal function or by influence of other environmental factors. The aim of the study was to evaluate the possible mechanism for the development of salt-sensitive essential hypertension in the population of Georgia. The Case-Control study included 185 subjects, 94 cases with Essential Hypertension stage I (JNC7) without prior antihypertensive treatment, and 91 controls. Salt-sensitivity test was used to divide both case and control groups into salt-sensitive (n=112) and salt-resistant (n=73) subgroups. Endogenous cardiotonic steroids, sodium and PRA were measured in blood and urine samples at the different sodium conditions. Determinations of circulating levels of endogenous sodium pump inhibitors and PRA were carried out using the ELISA and RIA methods. Descriptive statistics were used to analyze the data. Differences in variables between sodium conditions were assessed using paired t-tests. Salt-sensitivity was found in 60.5% of total population investigated, with higher frequency in females. Salt-sensitivity positively correlated with age in females (r=0.262, p<0.01). Statistically significant positive correlation was found between 24 hour urine sodium concentration changes and salt-sensitivity r=0.334, p<0.01. Significant negative correlation was found between salt-sensitivity and PRA. Since no significant correlations were found between BMI and salt-sensitivity, we assume that BMI and salt-sensitivity should be discussed as different independent risk factors for the development of Essential Hypertension. Significant correlation was found between changes in GFR in salt-sensitive cases and controls p<0.01. This can be explained with comparable hyperfiltration of the kidneys at high sodium load and discussed as early sign of hypertensive nephropathy in salt-sensitive individuals. At the high sodium condition Endogenous MBG and OU were high in salt-sensitive subjects compared to salt-resistant. These compounds decreased after low salt diet in salt-sensitive cases as well as controls but remained within the same level in salt-resistant individuals. MBG and OU levels positively correlated with SBP in salt-sensitive individuals but salt-resistant subjects didn't show any changes. Our results support the idea that chronic high sodium loading (>200 mmol) which is typical in traditional Georgian as well as other diets switch those humoral and pathophysiological mechanisms that can lead to the development of certain type of hypertension in salt-sensitive individuals. Salt intake reduction can prevent development of hypertension in salt-sensitive subjects, although hypertension develops in the salt-resistant individuals but by other mechanism such as RAAS." @default.
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• W2544512911 date "2016-09-01" @default.
• W2544512911 modified "2023-09-23" @default.
• W2544512911 title "POSSIBLE MECHANISM OF DEVELOPMENT OF SALT SENSITIVE ESSENTIAL HYPERTENSION." @default.
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