Exchangeable and Total Body Sodium and Potassium in Various Hypertensive Syndromes

2015 ◽  
pp. 169-178 ◽  
Author(s):  
J. I. S. Robertson ◽  
C. Beretta-Piccoli ◽  
K. Boddy ◽  
J. J. Brown ◽  
A. M. M. Cumming ◽  
...  
Keyword(s):  
Body Sodium ◽  
Total Body ◽  
Sodium And Potassium

scholarly journals Osmotically inactive sodium and potassium storage: lessons learned from the Edelman and Boling data

2016 ◽  
Vol 311 (3) ◽  
pp. F539-F547 ◽  
Author(s):  
Minhtri K. Nguyen ◽  
Dai-Scott Nguyen ◽  
Minh-Kevin Nguyen
Keyword(s):  
Linear Regression ◽  
Measurement Errors ◽  
Linear Regression Analysis ◽  
Sodium Concentration ◽  
Lessons Learned ◽  
Dynamic Changes ◽  
Data Set ◽  
Storage Pool ◽  
Total Body ◽  
Sodium And Potassium

Because changes in the plasma water sodium concentration ([Na+]pw) are clinically due to changes in the mass balance of Na+, K+, and H2O, the analysis and treatment of the dysnatremias are dependent on the validity of the Edelman equation in defining the quantitative interrelationship between the [Na+]pw and the total exchangeable sodium (Nae), total exchangeable potassium (Ke), and total body water (TBW) (Edelman IS, Leibman J, O'Meara MP, Birkenfeld LW. J Clin Invest 37: 1236–1256, 1958): [Na+]pw = 1.11(Nae + Ke)/TBW − 25.6. The interrelationship between [Na+]pw and Nae, Ke, and TBW in the Edelman equation is empirically determined by accounting for measurement errors in all of these variables. In contrast, linear regression analysis of the same data set using [Na+]pw as the dependent variable yields the following equation: [Na+]pw = 0.93(Nae + Ke)/TBW + 1.37. Moreover, based on the study by Boling et al. (Boling EA, Lipkind JB. 18: 943–949, 1963), the [Na+]pw is related to the Nae, Ke, and TBW by the following linear regression equation: [Na+]pw = 0.487(Nae + Ke)/TBW + 71.54. The disparities between the slope and y-intercept of these three equations are unknown. In this mathematical analysis, we demonstrate that the disparities between the slope and y-intercept in these three equations can be explained by how the osmotically inactive Na+ and K+ storage pool is quantitatively accounted for. Our analysis also indicates that the osmotically inactive Na+ and K+ storage pool is dynamically regulated and that changes in the [Na+]pw can be predicted based on changes in the Nae, Ke, and TBW despite dynamic changes in the osmotically inactive Na+ and K+ storage pool.

scholarly journals Relationships Among Intravascular Volume, Total Body Sodium, Arterial Pressure, and Vasomotor Tone

1961 ◽  
Vol 9 (6) ◽  
pp. 1233-1239 ◽  
Author(s):  
HIDEO TAKAGI ◽  
HARRIET P. DUSTAN ◽  
IRVINE H. PAGE
Keyword(s):  
Arterial Pressure ◽  
Intravascular Volume ◽  
Vasomotor Tone ◽  
Body Sodium ◽  
Total Body

scholarly journals Advances in understanding the role of cardiac glycosides in control of sodium transport in renal tubules

2014 ◽  
Vol 222 (1) ◽  
pp. R11-R24 ◽  
Author(s):  
Syed Jalal Khundmiri
Keyword(s):  
Heart Failure ◽  
Intracellular Signaling ◽  
Cardiac Contractility ◽  
Myocardial Cell ◽  
Renal Tubules ◽  
Intracellular Signaling Pathway ◽  
Body Sodium ◽  
Membrane Bound ◽  
Total Body

Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ATPase activity, cell signaling, and blood pressure regulation.

Free Amino Acid and Haemolymph Concentration Changes in Sphaeroma Rugicauda (Isopoda) During Adaptation to a Dilute Salinity

1969 ◽  
Vol 50 (2) ◽  
pp. 319-326
Author(s):  
R. R. HARRIS
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Free Amino Acid ◽  
Free Amino Acids ◽  
Free Amino ◽  
Sea Water ◽  
Protein Nitrogen ◽  
Body Sodium ◽  
Concentration Changes ◽  
Total Body

1. Non-protein and protein nitrogen fractions of the isopod Sphaeroma rugicauda were measured in animals adapted to 100 and 2% sea water. 2. The non-protein nitrogen component was reduced in animals acclimatized to the lower salinity. 3. Free amino acids accounted for 88 and 74% respectively of the non-protein nitrogen in the two salinities. 4. In 2% sea water taurine, proline, glycine, alanine and glutamic acid showed the greatest decreases in concentration compared to the levels measured in animals adapted to 100% sea water. 5. The decrease in total free amino acids of animals acclimatized to 100% sea water and transferred to 2% sea water was measured. 6. The total free amino acid concentration is reduced to the 2% sea water level within 12 hr. after transfer. 7. Free amino acid, haemolymph sodium and total body sodium levels after transfer to 2% sea water were compared. 8. The asymmetry between the fall in haemolymph sodium concentration and the decrease in total body sodium under these conditions is thought to be due to a water shift from the haemolymph into the tissues. 9. It is suggested that the osmotic pressure of the cells falls at a slower rate than that of the haemolymph.

Bone resorption and mineral excretion in rats during spaceflight

1983 ◽  
Vol 244 (3) ◽  
pp. R327-R331 ◽  
Author(s):  
C. E. Cann ◽  
R. R. Adachi
Keyword(s):  
Neutron Activation Analysis ◽  
Bone Resorption ◽  
Time Course ◽  
Large Change ◽  
Sodium Potassium ◽  
Total Body Calcium ◽  
Mineral Excretion ◽  
Synchronous Control ◽  
Total Body ◽  
Sodium And Potassium

Bone resorption was measured directly in flight and synchronous control rats during COSMOS 1129. Continuous tracer administration techniques were used, with replacement of dietary calcium with isotopically enriched 40Ca and measurement by neutron activation analysis of the 48Ca released by the skeleton. There is no large change in bone resorption in rats at the end of 20 days of spaceflight as has been found for bone formation. Based on the time course of changes, the measured 20–25% decrease in resorption is probably secondary to a decrease in total body calcium turnover. The excretion of sodium, potassium, and zinc all increase during flight, sodium and potassium to a level four to five times control values.

Changes in blood pressure and body sodium of rats fed sodium and potassium chloride

1961 ◽  
Vol 8 (4) ◽  
pp. 527-532 ◽  
Author(s):  
George R. Meneely ◽  
Janet Lemley-Stone ◽  
William J. Darby
Keyword(s):  
Blood Pressure ◽  
Potassium Chloride ◽  
Body Sodium ◽  
Sodium And Potassium

The Effects of Sodium Loading and Deprivation on Plasma Renin and Plasma and Urinary Aldosterone in Hypertension

1972 ◽  
Vol 42 (1) ◽  
pp. 15-23 ◽  
Author(s):  
J. P. Coghlan ◽  
A. E. Doyle ◽  
G. Jerums ◽  
B. A. Scoggins
Keyword(s):  
Excretion Rate ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Hypertensive Patients ◽  
Body Sodium ◽  
Sodium Load ◽  
Total Body

1. Measurements of urinary aldosterone excretion and of peripheral venous plasma concentrations of aldosterone, Cortisol and corticosterone have been made in hypertensive and normotensive patients after a sodium load and after dietary sodium restriction and ambulation. 2. Plasma concentrations of aldosterone, Cortisol and corticosterone did not differ significantly between the two groups of patients, but the rise in urinary aldosterone excretion was significantly greater in normotensive than in hypertensive patients after sodium restriction. 3. Division of the hypertensive patients into two groups according to the response in plasma renin on sodium restriction did not disclose any significant differences between responders and non-responders in respect of aldosterone or Cortisol, but the plasma corticosterone rose more in normotensive patients after sodium depletion than in the unresponsive hypertensive patients. 4. It is concluded that both the rise in plasma renin and in aldosterone excretion rate are blunted in hypertensive patients after sodium restriction. It is suggested that this may be due to a rise in total body sodium in hypertensive patients. 5. Differences in aldosterone excretion rate are not reflected in the values of peripheral venous concentrations, presumably because of the short-term rise in plasma aldosterone which results from ambulation.

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