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Biomedical subjects

A M Heagerty

Publications and source records attributed to A M Heagerty.

At least 127 records · Page 7Linked to original sources
PubMed1987

Abnormalities of erythrocyte membrane fatty acid composition in human essential hypertension.

The fatty acid content of erythrocyte plasma membrane was estimated in cells of 17 untreated hypertensive patients, and compared to that of 16 control subjects matched for age, sex and weight. Mean linoleic acid (18:2) content was significantly lower in hypertensives than controls, whereas arachidonic acid (20:4) and oleic acid (18:1) were significantly higher. These results provide further evidence for an alteration in the physiochemical structure of the plasma membrane in cells of hypertensive patients and may be related to the multiple disturbances in erythrocyte ion fluxes which have been observed.

Erythrocyte Membrane↗
PubMed1986

Influence of dietary linoleic acid on leucocyte sodium transport and blood pressure.

In a randomised double blind study to determine whether an increase in the polyunsaturated fat linoleic acid might influence leucocyte membrane sodium transport 22 normotensive volunteers received an oral supplement of linoleic acid or placebo daily for four weeks. Mean total sodium efflux rose significantly during supplementation with linoleic acid compared with placebo. In addition, all components of lying and standing blood pressure fell, though only the fall in supine systolic pressure was significant. Dietary supplementation with linoleic acid may alter ion fluxes across the cell membrane, presumably through changes in its physicochemical structure. In addition, the change in fat intake may lower blood pressure, though to only a very modest extent.

Biological Transport↗
PubMed1986

Cell membrane sodium transport: a correlation between human resistance vessels and leucocytes.

Sodium efflux was studied in leucocytes and resistance vessels from omental fat from 18 subjects undergoing laparotomy. The efflux of sodium was considerably faster from resistance vessels than from leucocytes, but there was a significant correlation between total efflux rate constants in the two tissues. This was attributable to a highly significant correlation between active sodium pumping as assessed by the ouabain-sensitive sodium efflux rate constants observed in both tissues. These results indicate that intrinsic characteristics of cell membrane electrolyte transport are shared by the leucocyte and vascular smooth muscle in human beings. Therefore, leucocytes can be used to provide information about altered vascular ion handling.

Aged↗
PubMed1986

Intravenous infusion of magnesium sulphate after acute myocardial infarction: effects on arrhythmias and mortality.

Two hundred patients with acute myocardial infarction were entered into a randomised double-blind trial where they received either intravenous magnesium sulphate or saline for 24 hours after admission to hospital. The incidence of ventricular arrhythmias necessitating treatment was reduced by more than half in the group receiving magnesium sulphate. There were two deaths in the group receiving magnesium sulphate and seven receiving saline placebo. Total cardiac events were significantly reduced in the magnesium treated group. These reductions cannot be attributed to differences in risk factors or therapy between the two groups, either before or during the period of study. These results suggest that magnesium administration reduces the incidence of serious tachyarrhythmias and death after acute myocardial infarction and that this simple regime warrants further study.

Arrhythmias, Cardiac↗
PubMed1986

Ion transport in hypertension: are changes in the cell membrane responsible?

Disturbances in several, distinct cell membrane ion transport processes have been demonstrated in essential hypertension but their variable relationship to blood pressure in different populations has made it difficult to achieve a unifying hypothesis. We suggest that altered composition of the lipid fraction of the cell membrane is the common underlying factor. This would produce many of the reported perturbations of cell membrane properties and function, not all of which relate directly to the development of hypertension, but which act as markers for the underlying abnormality. However, functions such as phosphoinositol turnover, calcium binding and Ca2+,Mg2+-ATPase dependent calcium efflux, which are influenced by the lipid composition of the membrane, provide a possible link between the membrane disturbance, intracellular calcium, vascular smooth muscle contraction and blood pressure. Alteration in the lipid content of the cell membrane not only provides an explanation for the variability in the ion transport abnormalities between populations but perhaps also for some of the variability in blood pressure within a single population. It also provides a potential means of influencing blood pressure by dietary intervention.

Animals↗
PubMed1986

Effects of changes in sodium balance on leucocyte sodium transport: qualitative differences in normotensive offspring of hypertensives and matched controls.

To investigate the effects of changes in sodium balance on blood pressure and leucocyte sodium transport, normotensive first-degree relatives of hypertensive patients and control subjects were randomized to receive low- and high-salt diets for 2 weeks, separated by a wash-out period of 2 weeks. High-salt intake failed to alter blood pressure, whereas the low-salt diet produced significant falls in standing pressures in both groups. In the control subjects leucocyte sodium efflux was not changed by either manoeuvre, but in the relatives low-salt diet stimulated ouabain-insensitive sodium efflux rate constant. There was a significant qualitative difference in the pattern of response of total efflux rate constant to the two dietary periods between the two groups of subjects. These data are not compatible with the release of a humoral sodium pump inhibitor in response to sodium-induced volume expansion, and lend support to a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.

Analysis of Variance↗
PubMed1986

Abnormal vascular phosphoinositide hydrolysis in the spontaneously hypertensive rat.

The production of [3H]-inositol phosphates was studied in labelled segments of aorta from spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) controls at 5 and 19 weeks, either unstimulated or in the presence of noradrenaline. Basal hydrolysis of inositol phospholipids was significantly enhanced in young SHR (P less than 0.05) compared to controls but this difference was no longer detected at 19 weeks. Noradrenaline increased [3H]-inositol phosphate accumulation in both SHR and WKY, but maximal hydrolysis was significantly greater in WKY (P less than 0.01), although the ED50 was similar in both groups of animals. These data demonstrate that phosphatidylinositide hydrolysis is enhanced in the young hypertensive rat at the time blood pressure is rising, but that this activity has declined by the time hypertension has reached an established phase. In addition, alpha 1-agonist induction of inositol phospholipid hydrolysis differs in the two species of animals, being reduced in genetically mature hypertensive rats.

Aging↗
PubMed1986

Leukocyte ionized calcium and sodium content and blood pressure in humans.

The relationship between leukocyte ionized calcium concentration, sodium content, and blood pressure was studied in normotensive subjects with (n = 17) and without (n = 21) a family history of hypertension and in untreated patients with essential hypertension (n = 22). There was a highly significant correlation between intracellular ionized calcium and mean supine blood pressure (measured on the same occasion) in normal subjects with no family history of hypertension (r = +0.73, p less than 0.01). This relationship was lost in normal subjects with a family history of hypertension, and in hypertensive patients there was a nonsignificant negative correlation between intracellular ionized calcium and blood pressure (r = +0.08 and -0.31, respectively). Intracellular ionized calcium was similar in the normotensive groups (both, 126 +/- 7 nmol/L) and slightly but nonsignificantly elevated in hypertensive patients (143 +/- 10 nmol/L; p = 0.09). There was no correlation between intracellular ionized calcium and sodium content in any group (r less than 0.1). These results indicate that while leukocyte ionized calcium in normotensive subjects with no family history of hypertension may reflect smooth muscle contractility resulting in the positive correlation between leukocyte ionized calcium and blood pressure, this relationship is lost in hypertensive patients and subjects predisposed to hypertension. This may be due to an altered relationship between leukocyte and smooth muscle calcium handling in these subjects or to non-calcium-mediated influences on blood pressure.

Adult↗
PubMed1986

Erythrocyte membrane calcium binding in normotensive and hypertensive subjects.

Calcium binding to erythrocyte membranes has been determined in patients with essential hypertension (EHT) and normotensive subjects with (NT + FH) and without (NT - FH) a family history of hypertension, to investigate its relationship to high blood pressure. The calcium content of erythrocyte membranes was measured by atomic absorption spectrophotometry after incubation in 0 (basal) or 40 mmol/l (maximal binding) calcium chloride. Basal calcium binding was reduced to a similar extent in both EHT and NT + FH subjects (11.4 +/- 0.5 and 10.9 +/- 0.9 mumol/g protein versus 13.7 +/- 0.6 mumol/g protein in NT - FH, P less than 0.01 for both). Maximal binding showed a similar pattern. These data suggest that cell membrane calcium binding is not directly related to blood pressure elevation but is the result of an inherited cell membrane defect which is present in essential hypertension patients and their relatives and which affects several membrane functions.

Blood Pressure↗
PubMed1985

Treatment of essential hypertension: changes in blood pressure, echocardiography and electrocardiography on three therapeutic regimes.

Forty-three patients with essential hypertension were randomly allocated to one of the following treatment regimes; - atenolol, atenolol and hydralazine or methyl dopa. Blood pressure fell into the normal range at 3 months and was similar in all 3 groups. Blood pressure remained controlled over the period of study. M-mode echocardiography was assessed initially, at 3, 6 and 12 months. All groups showed a fall in the measured indices towards the normal range with a significant reduction in left ventricular wall thickness at 3 months in the methyl dopa group and left ventricular mass in the atenolol group alone of 6 months. In conclusion, no one treatment regime appeared to have sustained advantages over another and none of the groups showed any deterioration on echocardiographic criteria during the study.

Adult↗
PubMed1984

Noradrenaline: a circulating inhibitor of sodium transport.

Leucocytes were isolated from venous blood of 11 normotensive volunteers with no family history of hypertension and the sodium efflux rate constants determined both alone and in the presence of increasing physiological concentrations of noradrenaline. There was a significant dose dependent reduction of total sodium efflux rate constant due to a reduction in ouabain sensitive sodium pump activity, glycoside insensitive efflux rate constants being unaffected. The magnitude of this effect was similar to the reduction in leucocyte sodium efflux rate constants observed in hypertensive patients (and their normotensive relatives). The noradrenaline induced depression of sodium pump activity was prevented by propranolol in a further seven experiments, suggesting that the effect was mediated by beta adrenoceptors. Catecholamines possibly functioning as circulating inhibitors of sodium transport may contribute to some of the disturbances in membrane electrolyte handling both in essential hypertension in man and in some experimental models of hypertension.

Biological Transport, Active↗
PubMed1984

Effects of treatment for hypertension on cerebral haemorrhage and infarction.

One hundred and sixty nine patients admitted to hospital for stroke over 30 months were examined to see whether treating hypertension had influenced the incidence of cerebral haemorrhage and infarction. Seventy eight (46%) of them had normal blood pressure, 47 (28%) previously diagnosed hypertension for which they were receiving treatment, and 44 (26%) previously undiagnosed and untreated hypertension. Haemorrhagic stroke was commoner among patients with untreated hypertension, whereas infarction was commoner in patients with treated hypertension. Infarction and haemorrhage were equally prevalent in patients with normal blood pressure. Effective treatment in this population seemed to have had a substantially different impact on vascular disease, giving rise to cerebral haemorrhage as opposed to infarction. This is consistent with evidence from other studies that treatment for hypertension has little or no effect on the progression of atheroma.

Aged↗