Reproducibility of salt sensitivity testing using a dietary approach in essential hypertension (original) (raw)
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American Journal of Hypertension, 1997
The ''gold standard'' for the assessment of salt pressure during the low Na diet (mean pressure Å 123 { 3 v 118 { 3 mm Hg; P õ .05). However, sensitivity of hypertension is the blood pressure response to dietary NaCl restriction; nevertheless, whereas patients identified as salt sensitive by the Grim protocol had a marked and significant blood for practical purposes, a more rapid test that would not depend on the patient's compliance to pressure decrease (systolic 012 mm Hg, diastolic 07 mm Hg) , no change was observed in those the dietary prescription would be very useful in clinical research and medical practice. The aim of classified as salt resistant (systolic 02 mm Hg, diastolic 02 mm Hg). A significant correlation this study was thus to evaluate the effectiveness and reliability of a rapid, easy-to-standardize between changes in urinary Na excretion and changes in blood pressure was found only in salt-protocol for the assessment of salt sensitivity against the blood pressure response to dietary salt sensitive hypertensive patients. In conclusion, the modified Grim protocol tested in this study was restriction. A total of 108 hypertensive patients were screened for salt sensitivity by the modified able to correctly predict a significant blood pressure response to dietary salt restriction in the protocol of Grim et al. Thereafter, nine patients identified by the test as salt sensitive and nine majority of cases. A validation of this test in a larger patient population may be advisable. identified as salt resistant followed, for two consecutive periods of 1 week, a diet with normal
American Journal of Hypertension, 1995
We used ambulatory blood pressure monitoring (ABPM) in the assessment of salt sensitivity in 40 essential hypertensive patients, comparing 24-h mean blood pressure during 7 days of low salt (20 mmol NaCl/day) and high salt (260 mmol NaC1/ day) intake. Salt sensitivity was diagnosed in 18 essential hypertensive patients (45%), each of them showing a significant increase in mean blood pressure (P < .05) from low to high salt diet. Salt-sensitive patients exhibited a high-salt--dependent increase in all blood pressure parameters including 24-h systolic, mean, diastolic blood pressure, blood pressure load, area under the curve, and awake and asleep blood pressure values. These patients exhibited a nondipper profile on both low-salt and high-salt diets. Salt-resistant patients (55%) showed a decrease in awake, and an increase in asleep blood pressure values after high salt intake, thus tending to flatten the circadian blood pressure profile. We conclude that ABPM is a useful method to assess salt sensitivity. In salt-resistant patients high salt intake induces a significant increase in asleep blood pressure with no significant changes in 24-h blood pressure, promoting a flattened blood pressure curve and tending to transform a dipper into a nondipper profile, which could have important implications in end-organ damage. Am J Hypertens 1995;8:970--977 KEY WORDS: Ambulatory blood pressure monitoring, salt sensitivity, blood pressure, circadian rhythm.
Clinical Science, 1996
1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin—aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-densi...
Salt Sensitivity and Hypertension
Hypertension Journal, 2017
Enough evidence is there to link excess salt intake with cardiovascular and renal risks through hypertension though substantial evidence is also there to support that blood pressure is not always responding to salt. A lot of metabolic and neurohormonal factors determine this salt sensitivity in addition to genetic factors that determine substantial excretion of salt, so it may not increase blood pressure despite high intake. Salt-sensitive hypertensives have reduced levels of urinary endothelin, contributing to impaired natriuresis in response to a salt load. Salt load also increases free radicals and paradoxically decreases excretion of nitric oxide metabolites in salt-sensitive individuals. Type 2 diabetic patients with microalbuminuria are more salt sensitive as they have lower urinary excretion of nitric oxide. Nitric oxide deficiency facilitates endothelial dysfunction causing hypertension in salt-sensitive people, impeding vasodilation after salt load. Sympathetic nervous system plays a significant role in maintenance of blood pressure in response to salt through urinary and plasma levels of catecholamine and renal nerve activity. Apart from this, atrial natriuretic peptides (ANPs) and cytochrome P450-derived metabolites of arachidonic acid play significant roles. Insomnia and menopause increase salt sensitivity. Kidney provides sensitive and specific biomarkers for salt sensitivity in the form of proteomics, and renal proximal tubule cells, microribonucleic acid (miRNA), and exosomes are excreted into the urine apart from genetic biomarkers. A J-shaped curve relationship exists between salt intake and mortality. Salt intakes above and below the range of 2.5 to 6.0 gm/day are associated with high cardiovascular risk. Salt restriction can be a cause of hypertension in inverse salt-sensitive people. Available prevalence studies do not differentiate between salt-sensitive and salt-resistant populations, nor do they include normotensive salt-sensitive people who get their blood pressure raised in response to dietary salt. In these circumstances, salt sensitivity arises as an independent risk factor for cardiovascular mortality and morbidity.
Salt sensitivity in hypertension. Renal and cardiovascular implications [clinical conference]
Hypertension, 1994
The mechanisms responsible for the increase in blood pressure response to high salt intake in salt-sensitive patients with essential hypertension are complex and only partially understood. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for such patients to retain salt and develop salt-dependent hypertension. The possible role of vasodilator and natriuretic agents, such as the prostaglandins, endothelium-derived relaxing factor, atrial natriuretic factor, and kinin-kallikrein system, requires further investigation. An association between salt sensitivity and a greater propensity to develop renal failure has been described in certain groups of hypertensive patients, such as blacks, the elderly, and those with diabetes mellitus. Salt-sensitive patients with essential hypertension manifest a deranged renal hemodynamic adaptation to a high dietary salt intake. During a low salt diet, salt-sensitive and salt-resistant patients have similar mean arterial pressure, glomerular filtra
Salt sensitivity: Concept and pathogenesis
Diabetes Research and Clinical Practice, 1998
Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, was described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the kidneys to excrete the whole intake of sodium until renal perfusion pressure (mean blood pressure) attains a level that is able to restore pressure-natriuresis relationship to values that enable the kidney to excrete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin system or endothelial function. It is also relevant that organ damage secondary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be significantly higher when compared with that of salt-resistant animals or humans. Interestingly, in humans, salt sensitivity has been shown to correlate with microalbuminuria, an important predictor of cardiovascular morbidity and mortality, which correlates with most of the cardiovascular risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high blood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypertensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanisms underlying the increase in BP, when salt intake is increased. Furthermore, therapy must preferably improve the diminished insulin sensitivity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk.
Salt restriction among hypertensive patients: Modest blood pressure effect and no adverse effects
Scandinavian Journal of Primary Health Care, 2009
Objective. Previous studies, mainly evaluating short-term very low salt diets, suggest that salt restriction may influence glucose and insulin metabolism, catecholamines, renin, aldosterone, and lipid levels adversely. The authors wanted to explore whether sodium restriction for eight weeks influenced insulin secretion unfavourably, and evaluate the efficacy and safety of such treatment also in terms of other parameters important in the management of hypertensive patients. Design. A double-blind randomized controlled parallel group designed trial. All participants received dietary advice aimed at a moderate salt-restricted diet. Half of the participants received salt capsules, the others received identical placebo capsules. Setting. General practice. Subjects. Forty-six hypertensive patients inadequately controlled by drug treatment. Main outcome measures. Fasting serum insulin C-peptide and glucose and levels of these measures after oral glucose, blood pressure, serum aldosterone and lipids, peripheral resistance, and skin conductance. Results. Salt restriction did not influence glucose and insulin metabolism, aldosterone, or lipid levels adversely. We observed better blood pressure regulation in the low salt group than in the high salt group, with a systolic and diastolic blood pressure difference of 5/5 mmHg after eight weeks. The difference was only statistically significant for diastolic blood pressure, p 0.02. Conclusion. This study revealed a modest diastolic blood pressure reducing effect of moderate sodium restriction. This reduction was obtained without any apparent unfavourable side effects such as increased insulin secretion, impaired glucose tolerance or dyslipidaemia.