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D N Baron

Publications and source records attributed to D N Baron.

At least 19 recordsLinked to original sources
PubMed1992

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International System of Units↗
PubMed1988

Effect of beta-blockade and subsequent triiodothyronine administration on human leucocyte Na-K ATPase.

We have investigated the effect of beta-blockade and beta-blockade + triiodothyronine (T3) administration on 86Rb (K) influx and [3H]-ouabain binding by human leucocytes and on plasma potassium concentrations. beta-blockade with nadolol (40 mg daily) for five days resulted in a significant decrease in 86Rb influx and [3H]-ouabain binding, as well as an increase in plasma potassium concentration. T3 administration thereafter caused a fall in plasma concentration and an increase in 86Rb influx. There was a tendency toward restoration of [3H]-ouabain binding to normal. The fact that beta-blockade inhibits 86Rb (K) influx and increases plasma potassium concentration implies that endogenous adrenaline exerts a tonic stimulatory effect upon 86Rb (K) influx and a suppressive effect on plasma potassium concentrations in vivo. T3 administration induces an increase in 86Rb (K) influx and a fall in plasma potassium concentrations. This suggests that either the effect of T3 is independent of beta-adrenoceptors or that the known increase in beta-adrenoceptor population secondary to T3 administration increases sensitivity to circulating adrenaline in spite of beta-blocker administration.

Adrenergic beta-Antagonists↗
PubMed1988

Effect of glucose intake on human leucocyte 86Rb influx and [3H]-ouabain binding.

86Rb influx and [3H] ouabain binding by human leucocytes were measured in eight normal nonobese fasting subjects before and after a challenge with 75 g glucose orally. The mean ouabain-sensitive 86Rb influx increased significantly from 194 to 283 mmol/kg protein/h (P less than .01), and [3H]-ouabain binding increased from 236 to 403 fmol/mg protein. The mean plasma potassium concentration fell from 4.2 to 3.9 mmol/L (P less than .05). Following intravenous glucose infusion, the median 86Rb transport increased from 186 to 267 mmol/kg protein/h, while median plasma potassium concentration fell from 4.3 to 3.9 mmol/L. Therefore, glucose intake acutely increases Na-K ATPase units, stimulates potassium (Rb) transport, and causes a concomitant fall in plasma potassium concentrations. Nutritional intake is probably an important determinant of Na-K ATPase units and activity in the human leucocyte.

Adult↗
PubMed1987

Increased leucocyte Na-K ATPase in obesity: reversal following weight loss.

Ouabain-sensitive 86Rb influx and [3H] ouabain binding capacity were investigated in the leucocytes of 17 obese patients and 15 control subjects. Both were significantly increased in the obese when compared with controls. Following dietary restriction and a 4% to 5% weight reduction in the obese over 2 weeks, [3H] ouabain binding and ouabain-sensitive 86Rb influx (a model for K+ influx) decreased to levels similar to those in controls. This shows that the number of Na-K ATPase sites on leucocyte membranes of the obese are significantly increased and that this is associated with accelerated 86Rb transport. Since both of these indices decreased following 4% to 5% reduction in body weight while the patients were still obese, increased Na-K ATPase is neither a marker of nor cardinal to the pathogenesis of obesity. We conclude that (1) increase in Na-K ATPase units and 86Rb influx are not characteristic of obesity itself and (2) dietary restriction over the short-term with limited weight reduction restores Na-K ATPase units and 86Rb influx to normal.

Adult↗
PubMed1987

Ion flux and Na+,K+-ATPase activity of erythrocytes and leucocytes in thyroid disease.

In hyperthyroidism, erythrocytes show decreased Na+,K+-ATPase activity, decreased [3H]ouabain binding capacity (an index of the number of sodium pumps) and decreased active sodium and potassium flux rates, with a high intracellular sodium concentration. As erythrocytes are non-nucleated and atypical cells, we have studied electrolyte status in thyroid disease using mixed leucocytes as well; the results obtained differed from those in erythrocytes. When compared with findings in healthy subjects, leucocyte Na+,K+-ATPase activity, [3H]-ouabain binding capacity, total and active rubidium (used instead of potassium) influx were all significantly increased in untreated hyperthyroidism and decreased in untreated hypothyroidism. In hyperthyroidism, there was also a decrease in plasma potassium, an increase in sodium efflux rate and efflux rate constant, but no significant changes in cell sodium and potassium concentrations. All these changes returned to normal in successfully treated patients. There was a significant correlation between these abnormalities of electrolyte status and thyroid disease status (as serum thyroid stimulating hormone and free thyroxine).

Adult↗
PubMed1987

Lack of effect of acute ethanol consumption on active cation fluxes of leucocytes and erythrocytes in healthy humans.

1. Acute ethanol consumption in human volunteers did not appear to alter active cation fluxes by Na+,K+-ATPase, or intracellular electrolyte concentrations, in peripheral leucocytes or erythrocytes. 2. Urinary electrolyte excretion was decreased after ethanol consumption, compared with controls. 3. Neither plasma glucose nor serum insulin was altered by ethanol. 4. After ethanol consumption there was an elevation of endogenous plasma adrenaline levels. This was accompanied by a leucocytosis, which could be attributed to a raised neutrophil count. 5. The raised adrenaline levels were not associated with hypokalaemia. 6. It is possible that in vivo ethanol may prevent adrenaline-induced hypokalaemia by fluidizing the membrane and/or decreasing the affinity of beta-receptors for adrenaline.

Adult↗
PubMed1987

Effect of short term triiodothyronine administration on human leukocyte Rb(K) influx and Na efflux.

The effect of short term T3 administration on leukocyte ouabain-sensitive 86Rb(K) influx and Na efflux in normal subjects was investigated. At a dose of 60 micrograms daily for 7 days, T3 induced a significant increase in leukocyte 86Rb(K) influx and a significant fall in plasma K concentrations. Plasma and intracellular Na concentrations did not change. [3H]Ouabain binding, a measure of Na-K ATPase units, did not change. A week after T3 administration, 86Rb(K) influx, Na efflux, and plasma K concentrations were normal. In a series of five hyperthyroid patients, both ouabain-sensitive 86Rb influx and [3H]ouabain binding were significantly greater than in normal subjects. We conclude that T3 stimulates 86Rb(K) influx and Na efflux by leukocytes in vivo independently of [3H]ouabain binding and that this increase is rapidly reversible. However, in hyperthyroid patients both 86Rb influx and [3H]ouabain binding are increased, probably due to prolonged exposure to thyroid hormone excess.

Adult↗
PubMed1986

The acute in vitro effect of ethanol, its metabolites and other toxic alcohols on ion flux in isolated human leucocytes and erythrocytes.

Using isolated healthy human leucocytes and erythrocytes as model cells, we investigated the inhibitory effect of ethanol, its metabolites and of other toxic alcohols on the active fluxes of rubidium (Rb: equivalent to K) and sodium (Na), and on Na,K-ATPase activity. Ethanol (80 mmol X l-1) inhibited total and ouabain-sensitive 86Rb influx and 22Na efflux in leucocytes, this being dose-related for total, ouabain-sensitive and ouabain-insensitive fluxes at higher concentrations. In erythrocytes inhibition occurred at 20 mmol X l-1 for 86Rb influx, dose-related at higher concentrations as for leucocytes. 22Na efflux was inhibited at 80 mmol X l-1 and above. Acetaldehyde (0.1 and 0.2 mmol X l-1), 1,2-propanediol (0.8 mmol X l-1) and 2,3-butanediol (0.4 mmol X l-1) inhibited all fractions of 86Rb influx in erythrocytes, but not in leucocytes. Methanol, 2-propanol and 1,2-ethanediol (16 and 32 mmol X l-1) inhibited 86Rb influx in erythrocytes, but not in leucocytes. The order of potency was 2-propanol greater than 1,2-ethanediol greater than methanol. Na,K-ATPase activity was inhibited in lysed leucocyte and erythrocyte preparations only at very high concentrations of the alcohols--suggesting that inhibition is due to an alteration in membrane structure and not to a direct effect on the enzyme.

1-Propanol↗