Inflammatory markers in salt sensitive hypertension (original) (raw)
Increased Levels of Atherosclerosis Markers in Salt-Sensitive Hypertension
American Journal of Hypertension, 2006
Background: Salt sensitivity in essential hypertension is associated with both endothelial dysfunction and increased cardiovascular risk. We evaluated several serum markers of atherosclerosis and endothelial function in a group of essential hypertensive patients classified on the basis of their salt sensitivity.
Association between salt sensitivity and target organ damage in essential hypertension
2000
Cardiovascular events occur more frequently in sodium-sensitive patients with essential hypertension; recently, sodium sensitivity was shown to be a cardiovascular risk factor independently of other classic factors such as blood pressure and cigarette smoking This study examined the relationship between salt sensitivity status and target organ damage in hypertensive patients. Ninety-six patients (35 men, 61 women) with moderate essential hypertension were studied for salt sensitivity status and the presence of target organ damage, including hypertensive retinopathy, serum creatinine, creatinine clearance, and urinary albumin excretion (UAE). Four different patterns of left ventricular anatomic adaptation were identified by categorizing patients according to the values of left ventricular mass index and relative wall thickness by the means of echocardiography. Fortyfive (47%) patients were shown to be salt-sensitive, in contrast to 51 (53%) salt-resistant subjects. Serum creatinine and UAE were significantly higher in the group of salt-sensitive hypertensives (P < < .05 and P < < .001, respectively). Left ventricular mass index (LVMI), relative wall thickness (RWT), and left atrial index (LAI) were all significantly higher in the group of saltsensitive hypertensive patients. Concentric hypertrophy was significantly more prevalent in the salt-sensitive group (37.8% v 11.8%; P < < .01). The prevalence of hypertensive retinopathy in the salt-sensitive group was 84.4%, in contrast to 59.6% in the salt-resistant group (P < < .01). Multivariate regression analysis revealed salt sensitivity as a significant predictor of LVMI, RWT, and UAE, independently of age, body mass index, and mean blood pressure. In conclusion, salt-sensitive hypertensive patients are more prone to develop severe hypertensive target organ damage that may enhance their risk of renal and cardiovascular morbidity.
Mechanisms of Salt-Sensitive Hypertension
Current Hypertension Reviews, 2015
Hypertension and its consequences, including heart failure, stroke, and kidney disease, are responsible for substantial morbidity and mortality worldwide. Lifestyle changes, particularly sodium reduction, contribute to blood pressure control. However, not all individuals, whether normotensive or hypertensive, have the same susceptibility to the effects of salt. While a variety of approaches have been proposed to identify salt sensitive patients, there is no consensus for a definition of salt sensitivity and the precise mechanisms that explain their association are not yet fully understood. In this review we summarize the current understanding of the various pathophysiological mechanisms potentially involved in determining the salt sensitive phenotype. Genetic, neuronal, and immune alterations are reviewed. Additionally, we provide an update on the current knowledge of a new approach proposing the interstitium of the skin may act as a sodium reservoir. The role of dietary potassium on salt sensitive hypertension is also summarized.
Procalcitonin and the inflammatory response to salt in essential hypertension
Journal of Hypertension, 2013
Objectives: Inflammation is considered as a major effector of arterial damage brought about by salt excess in animal models. In a randomized, single masked, cross-over study in 32 uncomplicated essential hypertensive patients, we assessed the effect of a short-term low-salt diet on biomarkers of innate immunity [procalcitonin (PCT), interleukin-6, C-reactive protein, and tumor necrosis factor-a (TNF-a)], adiponectin (ADPN, an anti-inflammatory cytokine), and leptin.
Salt sensitivity and its implication in clinical practice
Indian Heart Journal, 2018
Hypertension (HTN) is a complex multi-factorial disease and is considered one of the foremost modifiable risk factors for stroke, heart failure, ischemic heart disease and renal dysfunction. Over the past century, salt and its linkage to HTN and cardiovascular (CV) mortality has been the subject of intense scientific scrutiny. There is now consensus that different individuals have different susceptibilities to blood pressure (BP)-raising effects of salt and this susceptiveness is called as salt sensitivity. Several renal and extra-renal mechanisms are believed to play a role. Blunted activity of the renin-angiotensinaldosterone system (RAAS), adrenal Rac1-MR-Sgk1-NCC/ENaC pathway, renal SNS-GR-WNK4-NCC pathway, defect of membrane ion transportation, inflammation and abnormalities of Na + /Ca 2+ exchange have all been implicated as pathophysiological basis for salt sensitive HTN. While salt restriction is definitely beneficial recent observation suggests that treatment with Azilsartan may improve salt sensitivity by selectively reducing renal proximal tubule Na + /H + exchange. This encourages the future potential benefits of recognizing and therapeutically addressing the salt sensitive phenotype in humans.
Angiotensin II, interstitial inflammation, and the pathogenesis of salt-sensitive hypertension
American Journal of Physiology-Renal Physiology, 2006
Transient administration of ANG II causes persistent salt-sensitive hypertension associated with arteriolopathy, interstitial inflammation, and cortical vasoconstriction; blocking the vascular and inflammatory changes with mycophenolate mofetil (MMF) prevents vasoconstriction. While infiltrating leukocytes during the salt-sensitive hypertension phase express ANG II, the functional role of ANG II during this phase is not known. We examined the acute effect of candesartan on renal hemodynamics during the established salt-sensitive hypertensive phase and related these findings to direct measurement of intrarenal ANG II and inflammatory cells in rats previously exposed to ANG II with or without MMF treatment. Sham controls were also examined. The administration of ANG II, followed by exposure to high-salt diet, resulted in hypertension, cortical vasoconstriction, an increase in interstitial inflammatory cells (44.8 ± 1.3 lymphocytes/mm2, and 30.8 ± 1.2 macrophages/mm2ANG II vs. 19.6 ± 2...
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
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 of Blood Pressure and Insulin Resistance
Frontiers in Physiology
Salt sensitivity of blood pressure (SSBP) is an independent risk factor for cardiovascular morbidity and mortality that is seen in both hypertensive and normotensive populations. Insulin resistance (IR) strongly correlates with SSBP and affects nearly 50% of salt sensitive people. While the precise mechanism by which IR and SSBP relate remains elusive, several common pathways are involved in the genesis of both processes, including vascular dysfunction and immune activation. Vascular dysfunction associated with insulin resistance is characterized by loss of nitric oxide (NO)-mediated vasodilation and heightened endothelin-1 induced vasoconstriction, as well as capillary rarefaction. It manifests with increased blood pressure (BP) in salt sensitive murine models. Another common denominator in the pathogenesis of insulin resistance, hypertension, and salt sensitivity (SS) is immune activation involving pro-inflammatory cytokines like tumor necrosis factor (TNF)-α, IL-1β, and IL-6. In ...