Calcium retention and increased vascular reactivity caused by a hypothalamic sodium transport inhibitor

1988 ◽  
Vol 75 (2) ◽  
pp. 197-202 ◽  
Author(s):  
M. Afzal Mir ◽  
Kevin Morgan ◽  
Stephen Chappell ◽  
Mark Lewis ◽  
Gillian Spurlock ◽  
...  
Keyword(s):  
Sodium Transport ◽  
Vascular Reactivity ◽  
Inhibitory Effects ◽  
Active Sodium ◽  
Sodium Potassium ◽  
Sodium Efflux ◽  
Calcium Retention ◽  
Active Sodium Transport ◽  
Transport Inhibitor ◽  
Hypothalamic Cells

1. Using a previously established method of isolating an active-sodium-transport inhibitor (ASTI) from hypothalamic cell culture medium, the inhibitor was isolated and partially purified from sequential passages through Sephadex G-25 and h.p.l.c, and its effects on de-endothelialized rabbit aortic strips were investigated. 2. ASTI caused a cumulative concentration-dependent increase in tension which reversed slowly after wash, and the wash showed an identical effect on fresh strips. 3. Ouabain, used as a control, also caused a concentration-dependent increase in tension which reached a plateau at a concentration of 10 mmol/l. Both ouabain and ASTI caused a significant potentiation of the vasoconstrictor effect of noradrenaline at concentrations of 1 nmol/l-0.1 mmol/l. 4. Both ASTI and ouabain caused a significantly greater (P < 0.01) calcium retention than control medium in aortic strips. 5. Incubation of ASTI with prolidase, chymotrypsin and carboxypeptidase A destroyed the vasoconstrictor effects as well as its inhibitory effects on sodium, potassium-dependent adenosine triphosphatase and sodium efflux from erythrocytes, but leucine aminopeptidase was ineffective. 6. These studies suggest that hypothalamic cells in culture release a peptidic inhibitor of active sodium transport which increases vascular reactivity, potentiates vasoconstrictor effects of noradrenaline and causes calcium retention.

RELEASE OF AN ACTIVE SODIUM TRANSPORT INHIBITOR (ASTI) FROM RAT HYPOTHALAMIC CELLS IN CULTURE

Endocrinology ◽  
1984 ◽  
Vol 115 (4) ◽  
pp. 1642-1644 ◽  
Author(s):  
KEVIN MORGAN ◽  
STEVEN M. FOORD ◽  
GILLIAN SPURLOCK ◽  
BAMBOS M. CHARALAMBOUS ◽  
CARLOS DIEGUEZ ◽  
...  
Keyword(s):  
Sodium Transport ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Cells In Culture ◽  
Transport Inhibitor ◽  
Hypothalamic Cells

Increase of lung sodium-potassium-ATPase activity during recovery from high-permeability pulmonary edema

1996 ◽  
Vol 271 (6) ◽  
pp. L896-L909 ◽  
Author(s):  
D. Zuege ◽  
S. Suzuki ◽  
Y. Berthiaume
Keyword(s):  
Atpase Activity ◽  
Pulmonary Edema ◽  
Sodium Transport ◽  
Sodium Ion ◽  
Type Ii ◽  
Active Sodium ◽  
Sodium Potassium ◽  
Sodium Ion Transport ◽  
Active Sodium Transport

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The purpose of these experiments was then to measure the activity of the sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-ATPase), the active component of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary edema in rats. Na(+)-K(+)-ATPase activity was significantly increased during recovery from lung edema. This increase could not be accounted for by the Na(+)-K(+)-ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of thiourea on the enzyme. Alveolar flooding, induced by instillation of a protein-containing solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-ATPase, suggesting that activation of the enzyme is probably secondary to either the presence of edema or the physiological consequences associated with edema. The quantity of lung Na(+)-K(+)-ATPase protein was also elevated during edema resolution, indicating that augmented synthesis of this enzyme underlies the increased enzyme activity observed. The quantity of Na(+)-K(+)-ATPase protein in alveolar type II cells was also significantly enhanced during recovery from edema, suggesting that these cells contribute to active sodium transport in vivo. The results of this study suggest that active sodium transport could participate in the resolution of pulmonary edema.

Cation Content and Transport Characteristics of the Sickle-Cell Erythrocyte and their Relationship with Structural Changes in the Membrane

1974 ◽  
Vol 46 (6) ◽  
pp. 679-692 ◽  
Author(s):  
J. Kurantsin-Mills ◽  
M. Kudo ◽  
S. Kojo Addae
Keyword(s):  
Sickle Cell ◽  
Sodium Transport ◽  
Structural Changes ◽  
Electron Microscopic Examination ◽  
Active Sodium ◽  
Electron Microscopic ◽  
Potassium Efflux ◽  
Thin Sections ◽  
Sodium Efflux ◽  
Active Sodium Transport

1. The intra-erythrocytic concentrations of sodium and potassium and the water content have been determined for haemoglobin (Hb) SS cells and negroid Hb AA cells. 2. The erythrocyte concentration of sodium was 40% higher and potassium 10% lower in the Hb SS than in the Hb AA cells. The cell water expressed as % weight of cell (corrected for trapped plasma) was identical for both cell types. 3. Normal Caucasian erythrocytes with Hb AA contained 40–50% less sodium but about the same potassium concentration as negroid Hb AA cells. 4. Potassium efflux into buffered iso-osmotic sucrose medium was much faster in Hb SS than in negroid Hb AA cells; ouabain-sensitive active sodium transport was twice as fast in the sickle-cell erythrocytes. Passive sodium efflux of erythrocytes suspended in a physiological medium was similarly faster in Hb SS cells. 5. Under the conditions of the experiments not less than 85% of the Hb SS erythrocytes appeared biconcave. Electron-microscopic examination of ultra-thin sections of Hb SS cells revealed marked discontinuities in the membrane. This suggests definite membrane alterations, which have probably resulted from the sickling-unsickling cycles occurring during the life-span of the cells. 6. It is suggested that the enhanced active sodium transport in the Hb SS erythrocyte is secondary to the augmented passive cation efflux, which in turn results from the leakiness of the erythrocyte membrane produced by the sickling-unsickling process.

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