Body Sodium (body + sodium)

Distribution by Scientific Domains

Kinds of Body Sodium

  • total body sodium


  • Selected Abstracts


    Loop Diuretics Can Cause Clinical Natriuretic Failure: A Prescription for Volume Expansion

    CONGESTIVE HEART FAILURE, Issue 1 2009
    Syed S. Ali MD
    Ultrafiltration enhances volume removal and weight reduction vs diuretics. However, their differential impact on total body sodium, potassium, and magnesium has not been described. Fifteen patients with congestion despite diuretic therapy had urine electrolytes measured after a diuretic dose. Ultrafiltration was initiated and ultrafiltrate electrolytes were measured. The urine sodium after diuretics (6047 mmol/L) was less than in the ultrafiltrate (1348.0 mmol/L) (P=.000025). The urine potassium level after diuretics (4123 mmol/L) was greater than in the ultrafiltrate (3.70.6 mmol/L) (P=.000017). The urine magnesium level after diuretics (5.23.1 mg/dL) was greater than in the ultrafiltrate (2.90.7 mg/dL) (P=.017). In acute decompensated heart failure patients with congestion despite diuretic therapy, diuretics are poor natriuretics and cause significant potassium and magnesium loss. Ultrafiltration extracts more sodium while sparing potassium and magnesium. The sustained clinical benefits of ultrafiltration compared with diuretics may be partly related to their disparate effects on total body sodium, potassium, and magnesium, in addition to their differential efficacy of volume removal. [source]


    Blood volume, blood pressure and total body sodium: internal signalling and output control

    ACTA PHYSIOLOGICA, Issue 1 2009
    P. Bie
    Abstract Total body sodium and arterial blood pressure (ABP) are mutually dependent variables regulated by complex control systems. This review addresses the role of ABP in the normal control of sodium excretion (NaEx), and the physiological control of renin secretion. NaEx is a pivotal determinant of ABP, and under experimental conditions, ABP is a powerful, independent controller of NaEx. Blood volume is a function of dietary salt intake; however, ABP is not, at least not in steady states. A transient increase in ABP after a step-up in sodium intake could provide a causal relationship between ABP and the regulation of NaEx via a hypothetical integrative control system. However, recent data show that subtle sodium loading (simulating salty meals) causes robust natriuresis without changes in ABP. Changes in ABP are not necessary for natriuresis. Normal sodium excretion is not regulated by pressure. Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Renin secretion is controlled by renal ABP, renal nerve activity and the tubular chloride concentrations at the macula densa (MD). Renal nerve activity is related to blood volume, also at constant ABP, and elevates renin secretion by means of ,1 -adrenoceptors. Recent results indicate that renal denervation reduces ABP and renin activity, and that sodium loading may decrease renin without changes in ABP, glomerular filtration rate or ,1 -mediated nerve activity. The latter indicates an essential role of the MD mechanism and/or a fourth mediator of the physiological control of renin secretion. [source]


    The brain angiotensin IV/AT4 receptor system as a new target for the treatment of Alzheimer's disease

    DRUG DEVELOPMENT RESEARCH, Issue 7 2009
    John W. Wright
    Abstract The brain renin-angiotensin system (RAS) regulates several physiologies including blood pressure, body sodium and water balance, cyclicity of reproductive hormones and related sexual behaviors, and the release of pituitary gland hormones. These physiologies are under the control of the angiotensin II (AngII)/AT1 receptor subtype system. The AngII/AT2 receptor subtype system is expressed during fetal development and is less abundant in the adult. This system appears to oppose growth responses facilitated by activation of the AT1 receptor. There is a growing list of nontraditional physiologies mediated by the most recently discovered angiotensin IV (AngIV)/AT4 receptor subtype system that include the regulation of blood flow, modulation of exploratory behaviors, involvement in stress responses and seizure, and a role in learning and memory acquisition. There is evidence to support an inhibitory influence by AngII, and a facilitory role by AngIV, on neuronal firing rate, long-term potentiation, and associative and spatial learning and memory. These findings suggest an important role for the RAS, and the AT4 receptor in particular, in normal cognitive processing and provide the stimulus for developing drugs that penetrate the blood-brain barrier to interact with this brain receptor in the treatment of dysfunctional memory. Drug Dev Res 70: 472,480, 2009. 2009 Wiley-Liss, Inc. [source]


    THE ,BODY FLUID PRESSURE CONTROL SYSTEM' RELIES ON THE RENIN,ANGIOTENSIN,ALDOSTERONE SYSTEM: BALANCE STUDIES IN FREELY MOVING DOGS

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005
    Erdmann Seeliger
    SUMMARY 1.,The physiological role of the ,renal body fluid pressure control system', including the intrarenal mechanism of ,pressure natriuresis', is uncertain. 2.,Balance studies in freely moving dogs address the following questions: (i) what is the physiological contribution of pressure natriuresis to the control of total body sodium (TBS); (ii) to what extent is long-term mean arterial blood pressure (MABP) determined by TBS and total body water (TBW); and (iii) during Na accumulation, is Na stored in an osmotically inactive form? 3.,Diurnal time-courses of Na excretion (UNaV) and MABP reveal no correlation. Spontaneous MABP changes do not affect UNaV. The long-term 20% reduction of renal perfusion pressure (RPP) results in Na retention via pressure-dependent stimulation of the renin,angiotensin,aldosterone system (RAAS), not via a pressure natriuresis mechanism. Prevention of pressure natriuresis does not result in ongoing Na retention when the RAAS is operative. The long-term 20% elevation of RPP induced by sustained TBS elevation facilitates Na excretion via pressure natriuresis, but does not restore TBS to normal. 4.,Changes in TBW correlate well with changes in TBS (r2 = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r2 = 0.91). 5.,With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r2 = 0.69). At lowered TBW, no correlation is found. 6.,In conclusion, the physiological role of pressure natriuresis is limited. Pressure natriuresis does not appear to be operative when RPP is changed from ,20 to +10% and neurohumoral control of UNaV is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on UNaV. Pressure natriuresis may constitute a compensating mechanism under pathophysiological conditions of substantial elevation of RPP. A large portion of the long-term changes in MABP are attributable to changes in TBW. The notion of osmotically inactive Na storage during Na accumulation appears to be invalid. [source]