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

Seven normal subjects were subjected to depletion and repletion of body potassium on balance regimen. Aldosterone excretion, plasma volume, and arterial pressure were measured. Potassium depletion decreased and potassium repletion consistently increased aldosterone excretion. Changes in sodium balance were prevented by restricting dietary sodium or replacing lost sodium. The effects on aldosterone excretion were thus shown to be independent of reciprocal changes in sodium balance of intravascular volume or of arterial pressure. The results suggest that changes in body potassium influence aldosterone secretion by mechanisms independent of those responsive to changes in body sodium or fluid volume.

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Relation of Arterial Pressure with Body Sodium, Body Potassium and Plasma Potassium in Essential Hypertension

Clinical Science ◽

10.1042/cs0630257 ◽

1982 ◽

Vol 63 (3) ◽

pp. 257-270 ◽

Cited By ~ 81

Author(s):

C. Beretta-Piccoli ◽

D. L. Davies ◽

K. Boddy ◽

J. J. Brown ◽

A. M. M. Cumming ◽

...

Keyword(s):

Essential Hypertension ◽

Arterial Pressure ◽

Potassium Concentration ◽

Plasma Potassium ◽

Normal Subjects ◽

Total Body Potassium ◽

Hypertensive Patients ◽

Body Sodium ◽

Low Renin Hypertension ◽

Total Body

1. Exchangeable sodium (NaE), plasma electrolytes and arterial pressure were measured in 121 normal subjects and 91 patients with untreated essential hypertension (diastolic >100 mmHg), 21 of whom had low-renin hypertension. Plasma concentrations of renin, angiotensin II and aldosterone were measured in all hypertensive patients, total body sodium, total body potassium and exchangeable potassium (KE) in some patients. 2. Mean NaE was not different in normal and hypertensive subjects provided the two groups were matched for leanness index. In the subgroup of young hypertensive patients aged 35 years or less mean NaE was below normal. NaE was not related to arterial pressure in normal subjects but in hypertensive patients there were positive and significant correlations of arterial pressure with NaE and with total body sodium. 3. NaE and total body sodium increased with age in hypertensive but not in normal subjects. Partial regression analysis suggested that the correlation of NaE with arterial pressure was not explained by an influence of age. 4. Mean NaE was not increased and mean KE was not decreased in patients with low-renin hypertension. 5. Plasma potassium concentration, KE and total body potassium correlated inversely and significantly with blood pressure in hypertensive patients. These correlations were more marked in young than in old patients. 6. Multiple regression analysis showed that the combination of NaE and plasma potassium concentration ‘explained’ more of the variation of systolic blood pressure in hypertensive patients than it did in normal subjects. Plasma potassium concentration ‘explained’ more of the variation in young hypertensives and NaE ‘explained’ more in older patients. 7. Our findings suggest that changes of plasma and body potassium are important in the earlier stages of essential hypertension and that changes of body sodium become important later.

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Relation of Arterial Pressure with Exchangeable and Total Body Sodium and with Plasma Exchangeable and Total Body Potassium in Essential Hypertension

Clinical Science ◽

10.1042/cs061081s ◽

1981 ◽

Vol 61 (s7) ◽

pp. 81s-84s ◽

Cited By ~ 9

Author(s):

C. Beretta-Piccoli ◽

D. L. Davies ◽

K. Boddy ◽

J. J. Brown ◽

A. M. M. Cumming ◽

...

Keyword(s):

Arterial Pressure ◽

Potassium Concentration ◽

Young Patients ◽

Plasma Potassium ◽

Normal Subjects ◽

Exchangeable Sodium ◽

Total Body Potassium ◽

Hypertensive Patients ◽

Body Sodium ◽

Total Body

1. Arterial pressure, plasma electrolytes and exchangeable sodium were measured in 91 patients with essential hypertension and in 121 normal control subjects. Total body sodium, exchangeable potassium and total body potassium were also measured in some of the hypertensive patients. 2. Mean plasma sodium concentration was slightly but significantly lower in the hypertensive patients as a group, but mean values for other electrolyte measurements were close to normal or predicted normal. 3. Exchangeable sodium was not related to arterial pressure in normal subjects but in hypertensive patients exchangeable sodium correlated significantly with systolic and diastolic pressures. These correlations were significant with two methods of expressing exchangeable sodium, in the whole group of patients, in men and in older patients. Exchangeable sodium was not significantly related to arterial pressure in young patients. 4. Total body sodium also correlated significantly with systolic and diastolic pressures in hypertensive patients. 5. Exchangeable sodium was significantly related to age in hypertensive patients but not in normal subjects. Mean exchangeable sodium was significantly lower than normal in young patients. 6. Plasma potassium concentration was not related to arterial pressure in normal subjects but in essential hypertensive patients plasma potassium concentration, exchangeable potassium and total body potassium correlated negatively with systolic and diastolic pressures. These correlations were also significant in young, but not in old patients.

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Toward an Integrative Concept of Control of Total Body Sodium

Physiology ◽

10.1152/physiologyonline.2000.15.6.319 ◽

2000 ◽

Vol 15 (6) ◽

pp. 319-325 ◽

Cited By ~ 7

Author(s):

H. Wolfgang Reinhardt ◽

Erdmann Seeliger

Keyword(s):

Arterial Pressure ◽

Regulatory Elements ◽

Body Water ◽

Major Determinant ◽

Pressure Balance ◽

Renin Angiotensin Aldosterone System ◽

Body Sodium ◽

Total Body ◽

Integrative Concept ◽

Atrial Receptors

Total body sodium (TBSodium) is a major determinant of body water and arterial pressure. Several observations, in particular that of a “sodium memory,” indicate that TBSodium is a controlled variable. Various regulatory elements are involved, e.g., the renin-angiotensin-aldosterone system, atrial receptors, and renal arterial pressure. Balance studies in dogs provide new insights into their contributions to TBSodium control.

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

Journal of Endocrinology ◽

10.1530/joe-13-0613 ◽

2014 ◽

Vol 222 (1) ◽

pp. R11-R24 ◽

Cited By ~ 5

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.

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

Journal of Experimental Biology ◽

10.1242/jeb.50.2.319 ◽

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.

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Pulmonary vasodilation to adrenomedullin: a novel peptide in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.6.h2211 ◽

1995 ◽

Vol 268 (6) ◽

pp. H2211-H2215 ◽

Cited By ~ 8

Author(s):

J. Heaton ◽

B. Lin ◽

J. K. Chang ◽

S. Steinberg ◽

A. Hyman ◽

...

Keyword(s):

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Vasomotor Tone ◽

Pulmonary Vasodilation ◽

Vascular Bed ◽

Pulmonary Vasodilator ◽

Vasodilator Activity ◽

Pulmonary Arterial ◽

Cgrp Receptor Antagonist ◽

Pulmonary Vascular Bed

The present study investigates the effects of human adrenomedullin (ADM) on the pulmonary vascular bed of isolated, blood-perfused rat lung. Because pulmonary blood flow and left atrial pressure were constant, changes in pulmonary arterial pressure directly reflect changes in pulmonary vascular resistance. Under conditions of resting (low) pulmonary vasomotor tone, intra-arterial bolus injections of ADM-(1-52) and two truncated sequences of ADM-(1-52) [ADM-(1-12) and ADM-(13-52)] did not alter pulmonary arterial pressure. When pulmonary vasomotor tone was increased by U-46619, a thromboxane A2 mimic, intra-arterial bolus injections of ADM-(1-52) and ADM-(13-52) at similar doses produced similar, dose-dependent reductions in pulmonary arterial pressure. On a molar basis, ADM-(1-52) had greater pulmonary vasodilator activity than isoproterenol. In contrast, ADM-(1-12) had no activity. When pulmonary vasomotor tone was actively increased to the same level using KCl, the pulmonary vasodilator activity of ADM-(13-52) was decreased 10-fold. The present data demonstrate that ADM-(1-52) dilates the pulmonary vascular bed and suggest that the pulmonary vasodilator activity of ADM is greater on pulmonary blood vessels preconstricted through a receptor-dependent mechanism. Because meclofenamate, nitro-L-arginine methyl ester, methysergide, BW A-1433U83, U-37883A, and calcitonin gene-related peptide [CGRP-(8-37)], a CGRP-receptor antagonist, did not alter the pulmonary vasodilator response to ADM-(1-52), the present data suggest that ADM dilates the pulmonary vascular bed independently of cyclooxygenase products, endothelium-derived relaxation factor, serotoninergic receptors, adenosine1 purinoreceptors, ATP-dependent potassium channels, and CGRP receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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Inhaled nitric oxide partially reverses hypoxic pulmonary vasoconstriction in the dog

Journal of Applied Physiology ◽

10.1152/jappl.1994.76.3.1350 ◽

1994 ◽

Vol 76 (3) ◽

pp. 1350-1355 ◽

Cited By ~ 18

Author(s):

J. A. Romand ◽

M. R. Pinsky ◽

L. Firestone ◽

H. A. Zar ◽

J. R. Lancaster

Keyword(s):

Nitric Oxide ◽

Arterial Pressure ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Hypoxic Pulmonary Vasoconstriction ◽

Canine Model ◽

Systemic Arterial Pressure ◽

Vasomotor Tone ◽

Pulmonary Vasoconstriction ◽

Pulmonary Arterial

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmonary vasomotor tone decreases pulmonary arterial pressure (Ppa). We conducted this study to better characterize the hemodynamic effects induced by NO inhalation during hypoxic pulmonary vasoconstriction in 11 anesthetized ventilated dogs. Arterial and venous systemic and pulmonary pressures and aortic flow probe-derived cardiac output were recorded, and nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) were measured. The effects of 5 min of NO inhalation at 0, 17, 28, 47, and 0 ppm during hyperoxia (inspiratory fraction of O2 = 0.5) and hypoxia (inspiratory fraction of O2 = 0.16) were observed. NO inhalation has no measurable effects during hyperoxia. Hypoxia induced an increase in Ppa that reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO induced an immediate (< 30 s) decrease in Ppa and calculated pulmonary vascular resistance (P < 0.05 each) but did not return either to baseline hyperoxic values. Increasing the concentration of NO to 74 and 145 ppm in two dogs during hypoxia did not induce any further decreases in Ppa. Reversing hypoxia while NO remained at 47 ppm further decreased Ppa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systemic arterial pressure. MetHb remained low, and NO-Hb was unmeasurable. We concluded that NO inhalation only partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective to the pulmonary circulation.

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