Search PubMed⌕ Search

Biomedical subjects

L Poston

Publications and source records attributed to L Poston.

At least 145 records · Page 8Linked to original sources
PubMed1985

Effect of the calcium antagonist verapamil on human leucocyte sodium transport in vitro.

Sodium efflux rate constants and intracellular sodium were measured in leucocytes from healthy volunteers in the presence and absence of the calcium antagonist verapamil hydrochloride. Verapamil stimulated sodium pump activity and this effect was dependent on the presence of external calcium. Verapamil has been reported to reverse the abnormality of sodium transport seen in leucocytes from patients with essential hypertension and the present study demonstrates that sodium pump activity in leucocytes from control subjects is also stimulated by exposure to verapamil in vitro. This direct cellular effect appears to be due to the calcium antagonist properties of the drug.

Biological Transport, Active↗
PubMed1985

Zinc abnormalities in fulminant hepatic failure.

Zinc is an important trace metal and, in liver disease, abnormal zinc metabolism has been reported. In this study of patients with fulminant hepatic failure progressing to grade IV encephalopathy, plasma zinc concentrations fell during the illness to reach levels significantly below normal; during this time urinary zinc excretion was markedly elevated.

Acetaminophen↗
PubMed1985

The effect of dietary sodium restriction on leucocyte sodium transport in normotensive subjects and in patients with essential hypertension.

Dietary sodium restriction (10 mmol Na/day) for a period of 2 weeks did not result in any change in the blood pressure of 12 healthy young adults (mean age 21). There was also no change in their leucocyte sodium transport investigated immediately before the diet and on the last day. Sodium restriction (10 mmol Na/day) in 12 middle-aged hypertensive subjects (mean age 56) for the same period of time caused a significant fall in both systolic and diastolic blood pressure. The leucocyte total sodium efflux rate constant was initially low, but after the diet significantly increased towards the control value. The results are compatible with the theory that a circulating sodium transport inhibitor is present in patients with essential hypertension, and is related to salt intake.

Adolescent↗
PubMed1984

Reversal by verapamil of defect in sodium transport in leucocytes in essential hypertension.

The effect of treatment with verapamil on cell sodium transport was studied in the leucocytes of patients with essential hypertension. Previously described abnormalities of sodium efflux rate constant and intracellular sodium content were confirmed, the component of the sodium efflux rate constant sensitive to ouabain being lower and the intracellular sodium content higher in the patients compared with controls. Verapamil reversed these abnormalities and reduced blood pressure.

Adult↗
PubMed1984

A circulating inhibitor of leucocyte sodium transport in patients with advanced liver cirrhosis.

Leucocyte sodium efflux was measured in control leucocytes pre-incubated for 90 min with serum from patients with advanced liver cirrhosis. Serum from patients with advanced alcoholic liver cirrhosis was inhibitory to sodium transport in control leucocytes. The degree of inhibition was similar to that seen in the patients' own leucocytes; the defect induced by patient serum was primarily inhibition of ouabain-insensitive sodium efflux, whereas in the patients' own leucocytes, inhibition was seen in both ouabain-sensitive and -insensitive sodium efflux, as shown previously. The results suggest that a circulating factor, present in patients with advanced cirrhosis, is capable of inhibiting sodium transport in leucocytes.

Adult↗
PubMed1984

Cellular sodium concentration and vasoconstrictor state in hypertension.

The sodium content of peripheral blood leucocytes was estimated in two separate investigations of the relationship between cellular sodium content and the vasoconstrictor state. In the first study various parameters of forearm blood flow were measured in a group of 31 normal subjects. A positive correlation was found between peripheral vascular resistance and leucocyte sodium content (p less than 0.05), and a negative correlation between venous compliance (VV60) and leucocyte sodium content (p less than 0.001). In the second study the leucocyte sodium content of 14 patients with essential hypertension was investigated before and after treatment with the calcium antagonist verapamil. The sodium content was found to be abnormally high, as previously described, and treatment with verapamil was found to reverse the defect. Both studies indicate a link between cell sodium content and the vasoconstrictor state, and the results are discussed in light of current theory.

Adult↗
PubMed1984

Sodium transport by leucocytes and erythrocytes in hypertensive subjects and their normotensive relatives.

Intracellular sodium content and ouabain-sensitive sodium efflux rate constant were measured in leucocytes and erythrocytes from subjects with untreated essential hypertension and also in normotensive subjects with and without a family history of hypertension. Leucocytes from hypertensives were again shown to have a higher intracellular sodium content and lower ouabain-sensitive sodium efflux rate constant than normotensive controls but there were no differences between those normotensive subjects with and those without a family history of hypertension. No differences in erythrocyte sodium content or efflux rate constant were seen between any of the three groups.

Adult↗
PubMed1983

The renin-angiotensin-aldosterone system in fulminant hepatic failure.

The relationship of the renin-angiotensin-aldosterone system to blood pressure and sodium homeostasis and to renal function was investigated serially in 12 patients with fulminant hepatic failure. The plasma concentrations of renin, angiotensin II, and aldosterone were, in most instances, markedly increased. Systolic blood pressure, which was often very low, showed a significant inverse relationship to the plasma renin concentration, suggesting that the marked stimulation of the system is a homeostatic response to hypotension. However, the plasma renin substrate concentration was markedly decreased, and the conversion of angiotensin II to inactive peptides increased, both of which may have severely limited the full 'expression' of the stimulated system. Renin and angiotensin II levels were both related to creatinine clearance, which was often reduced, but it is not clear as to which was cause and which effect. No relationship between the plasma aldosterone concentration and renal sodium excretion could be detected.

Adult↗
PubMed1983

Does potassium lower blood pressure by increasing sodium excretion? A metabolic study in patients with mild to moderate essential hypertension.

Potassium chloride (96 mmol potassium/day) in the form of 12 Slow K tablets/day in 10 patients on an intake of 150 mmol sodium and 80 mmol potassium produced a cumulative sodium loss of 110 mmol by the 12th day of potassium supplementation. At the same time there was attenuation of the expected increase in plasma renin activity appropriate for such a sodium loss. The lack of rise in plasma renin activity and hence angiotensin II combined with sodium loss may account at least in part for the observed blood pressure fall. No change in ouabain-sensitive or total white cell sodium efflux rate constant was found. An effect of an increase in plasma potassium on the sodium pump cannot be excluded as the white cell sodium efflux rate constant was measured in a fixed external potassium concentration. There was no evidence from plasma noradrenaline measurements that increasing potassium intake reduces sympathetic activity in the resting state.

Aldosterone↗
PubMed1982

Effects of serum from patients with fulminant hepatic failure on leucocyte sodium transport.

1. Serum from patients with fulminant hepatic failure inhibits the ouabain-sensitive sodium efflux in leucocytes. A 1 : 100 dilution of the serum was necessary before the inhibition became undetectable. 2. Dialysates of the serum through cuprophane in vitro and polyacrylonitrile haemodialysis in vivo were inhibitory in small amounts. 3. Ultrafiltrates ( less than 10 000 daltons) of serum were chromatographed on Sephadex G-25 and the elution profile obtained from patients with fulminant hepatic failure was both qualitatively and quantitatively different from that of normal controls. Material from peaks 3, 4, 5 and 7 in patients with fulminant hepatic failure inhibited leucocyte sodium transport. 4. dialysate from haemodialysis with the polyacrylonitrile membrane contained most peaks, particularly peaks 4 and 5. Adsorption of serum with polymer coated charcoal in vitro largely removed peaks 5-8.

Biological Transport↗
PubMed1982

Sodium transport during the natriuresis of volume expansion; a study using peripheral blood leucocytes.

1. Leucocyte sodium transport was investigated as a possible assay for the small molecular weight natriuretic material isolated from the urine of normal subjects who had undergone volume expansion by saline infusion. 2. This fraction (fraction four or FIV), inhibitory to sodium transport in several other assays, was also found to inhibit leucocyte sodium transport. 3. FIV isolated from the urine of five normal subjects undergoing the natriuresis of mineralocorticoid 'escape' was also found to be inhibitory to leucocyte sodium transport. 4. Leucocytes isolated from the blood of the same subjects during mineralocorticoid escape showed decreased sodium transport.

Adult↗
PubMed1981

Evidence for a circulating sodium transport inhibitor in essential hypertension.

The active sodium transport of white cells and red cells obtained from patients with essential hypertension was impaired. Incubating white cells from normotensive subjects in serum obtained from patients with essential hypertension caused an impairment in sodium transport in the white cells of normotensive subjects similar to that found in the white cells of hypertensive patients. The impairment in sodium transport was due to a fall in the ouabain-sensitive component of the total sodium efflux rate constant. These results show that the serum of patients with essential hypertension contains a substance which influences sodium transport and that it has ouabain-like activity. They also suggest that it is this substance which causes the impairment in sodium transport in the leucocytes of patients with essential hypertension. These findings support the hypothesis that the rise in blood pressure in patients with essential hypertension is due to an increased concentration of a circulating sodium transport inhibitor which is continuously correcting a tendency for sodium retention by the kidney.

Adult↗
PubMed1981

The effect of antihypertensive therapy on abnormal leucocyte sodium transport in essential hypertension.

Sodium transport in leucocytes of essential hypertensives was studied in physiological media. Untreated hypertensives have depressed values for the total and ouabain-sensitive sodium efflux rate constant. Treatment with diuretics abolished this abnormality. These results are compatible with the presence of a circulating inhibitor of sodium transport in essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1981

Abnormalities in the leukocyte sodium pump in advanced cirrhosis.

Previous studies have demonstrated abnormalities of intracellular electrolyte content and sodium transport in leukocytes of patients with fulminant hepatic failure. The current study was undertaken to establish whether similar abnormalities were present in patients with encephalopathy from advanced cirrhosis. Results from 19 patients with advanced cirrhosis showed values for the leukocyte total sodium efflux-rate constant were significantly reduced in patients, 3.02 +/- 1 SEM 0.12 h-1, compared to control values, 3.80 +/- 0.06 h-1. This reduction was due primarily to a lowering of the ouabain-sensitive component of sodium efflux, a measure of Na,K-ATPase activity. In comparison, leukocytes from patients with fulminant hepatic failure show a greater inhibition of the ouabain-sensitive component of sodium efflux with a raised ouabain-insensitive efflux. Although cirrhosis has generally been associated with potassium depletion, the intracellular potassium content of the cirrhotic patients' leukocytes was normal. Since the leukocyte is considered to be a good cell model and because abnormalities of sodium transport have been shown in the leukocytes of these patients, it is likely that similar abnormalities of sodium transport are present in other organs, including the brain.

Cholesterol↗