Body fluid compartments vascular endothelium11/28/2022 It also acts on ENaC in endothelia ( 7, 8), where it may cause the cell to swell ( 9, 10), stiffen ( 11, 12), and alter its output of nitric oxide ( 13– 15).īefore the experiments, endothelial cells were kept in two experimental conditions. This mineralocorticoid hormone is known to control the activity of epithelial sodium channels (ENaC) in the renal collecting duct. Salt and water balance is regulated by a multitude of factors/mediators, of which aldosterone is one of them. This internal sodium “escape” buffer, which is probably too small in humans with high blood pressure, indicates that extrarenal sodium balance plays an important role in blood pressure control ( 6). #Body fluid compartments vascular endothelium skin#In such individuals, the kidney has a limited ability to excrete the daily uptake of sodium and tends to retain the salt, most likely osmotically inactive, in skin and other extracellular compartments ( 5). Humans exposed to a high-salt diet may develop hypertension ( 4). The role of dietary salt in causing essential hypertension and other harmful cardiovascular effects, independent of blood pressure, derives from epidemiological studies, experimental models (particularly in primates), physiological and biochemical studies, controlled clinical trials, and genetic and mortality studies ( 3). The results suggest that changes in plasma sodium concentration per se may affect endothelial function and thus control vascular tone.Įssential hypertension is the sum of interactions between multiple environmental and genetic factors ( 1, 2). Nitric oxide formation was found down-regulated in cells cultured in aldosterone-containing high sodium medium. Lack of aldosterone in the culture medium or treatment with the epithelial sodium channel inhibitor amiloride prevented this response. The increase in stiffness occurred within minutes. Endothelial cell stiffness was unaffected by acute changes in sodium concentration <135 mM but rose steeply between 135 and 145 mM. The tip of an atomic force microscope was used as a nanosensor to measure stiffness of living endothelial cells incubated for 3 days in a culture medium containing aldosterone at a physiological concentration (0.45 nM). Because endothelial cells are ( i) sensitive to aldosterone, ( ii) in physical contact with plasma sodium, and ( iii) crucial regulators of vascular tone, we tested whether acute changes in plasma sodium concentration, within the physiological range, can alter the physical properties of endothelial cells. Recent observations suggest that a small increase in plasma sodium concentration may contribute to the pressor response of dietary salt. These differences are greatest in premature babies, when ECF exceeds ICF.Dietary salt plays a major role in the regulation of blood pressure, and the mineralocorticoid hormone aldosterone controls salt homeostasis and extracellular volume. The ICF volume is obtained by subtracting the ECF volume from the TBW.ĮCF exceeds 30% and ICF is <40%. The interstitial fluid volume is determined as the difference between ECF volume and plasma volume. These substances neither leave the vascular system nor penetrate the erythrocytes. Plasma volume can be measured either by radioactive albumin or by Evans blue. ECF volume is measured using inulin, which is proportionally distributed between plasma volume and interstitial volume. TBW is measured using deuterium oxide (heavy water). Vol1 = volume of indicator, Vol2 = volume to be measured.Īgents used for measurement of fluid compartments Relationship between the volumes of major fluid compartmentsĪ known amount of tracer is introduced into the space to be measured, and its concentration measured after mixing.Ĭon1 = initial concentration of indicator, Con2 = final concentration of indicator Total body water (TBW) constitutes 55-60% of the body weight in men and 45-50% of the body weight in young women.
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