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Biomedical subjects

R F Bing

Publications and source records attributed to R F Bing.

At least 37 records · Page 2Linked to original sources
PubMed1987

Failure of naloxone to influence surgical reversal of two-kidney, one-clip hypertension in the rat.

The rapid fall in blood pressure after removal of the constricting clip in two-kidney one-clip (2K-1C) hypertension in the rat is not fully explained by inhibition of the renin-angiotensin system or change in sodium balance. It has been postulated that compounds released in the renal venous effluent following unclipping of 2K-1C rats have a central opiate-like action and endogenous opioids are recognized to have profound hypotensive properties. To investigate this, we removed the clip from, or performed a sham operation in, early phase (less than 6 weeks) 2K-1C hypertensive rats during an infusion of naloxone, an opioid antagonist, or vehicle alone. The infusion of naloxone did not affect the pattern of blood pressure fall in either unclipped or sham-operated rats. Both naloxone-treated and control groups were similarly normotensive at 24 hr postoperation, the MAP being significantly lower than in the sham-operated groups, which regained previously hypertensive levels. Heart rate was unchanged 24 hr postoperatively in all groups. Morphine-induced bradycardia and hypotension were significantly reduced by naloxone infusion. Thus, naloxone infusion had no effect on blood pressure or heart rate in either the sham-operated or the unclipped groups, indicating that endogenous opioids do not have a major role in the reversal of renovascular hypertension under these circumstances.

Animals↗
PubMed1987

Nifedipine substituted for minoxidil in the treatment of refractory hypertension.

Nifedipine slow release tablets were substituted for minoxidil in the treatment of 13 patients with hypertension refractory to conventional therapy. In 12 patients substitution was associated with continuing control of blood pressure (BP), although 11 required maximum dose of 120 mg daily and one 80 mg daily. BP control remained satisfactory in nine patients for at least one year after substitution and in all, loop diuretics previously required with minoxidil to control fluid retention, were discontinued. Three patients (23%) however had to be withdrawn because of side effects; one within days of starting therapy and two after three months: one patient died after sustaining myocardial infarction. There was no evidence of deterioration in renal function in those patients continuing on nifedipine. This drug in combination with other antihypertensive agents provides an alternative approach to the management of patients with refractory hypertension, avoiding the severe side effects of the potent vasodilators.

Adrenergic beta-Antagonists↗
PubMed1987

Hydralazine sensitivity: clinical features, autoantibody changes and HLA-DR phenotype.

The clinical features, autoantibody changes, acetylator and HLA-DR phenotype of 20 patients with hydralazine-induced systemic lupus erythematosus are described. Four cases of particular interest are discussed in greater detail. Hydralazine sensitivity is more common in women, slow acetylators and the HLA-DR4 phenotype. Symptoms can occur even after many years of treatment and clinical awareness must be maintained for all patients to detect sensitivity at an early stage; there is no timely safe dose even in rapid acetylators. Joint symptoms predominate and full resolution is usual on discontinuing hydralazine. Failure of resolution should raise the suspicion of an underlying cause for the arthritis.

Acetylation↗
PubMed1987

Effects of manipulation of sodium balance on erythrocyte sodium transport.

The effects of changing sodium balance on blood pressure (BP) and erythrocyte sodium transport were investigated in normotensive first-degree relatives of hypertensive patients and control subjects randomised to receive low and high salt diets for two weeks, separated by a two week washout period. Changing from high to low salt intake produced a significant fall in standing diastolic pressure (DBP) in control subjects but not in the offspring of hypertensive patients. In both groups erythrocyte sodium efflux was not changed significantly by either manoeuvre, but the relatives had a significantly higher ouabain insensitive sodium efflux rate constant on both the low and the high salt diet compared to the controls (P less than 0.05). These results are not in keeping with the hypothesis which suggests the release of a humoral sodium pump inhibitor in response to sodium loading but lend support to the view that there is a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.

Adult↗
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

Neuropeptide Y in renovascular models of hypertension in the rat.

Neuropeptide Y content of the kidneys, heart, blood vessels, adrenals and brain stem was determined in both two-kidney, one-clip and one-kidney, one-clip Goldblatt hypertension in rats and compared with levels in age- and sex-matched controls. Renal neuropeptide Y content was significantly reduced in the clipped kidney of rats in both Goldblatt two-kidney, one-clip and Goldblatt one-kidney, one-clip models of hypertension. The content of neuropeptide Y was also reduced but to a lesser extent in the contralateral, non-ischaemic kidney in the two-kidney, one-clip model. In both models of hypertension, neuropeptide Y content in the heart was significantly reduced in the left ventricle and septum but unchanged in the atria and right ventricle wall. There was no significant change in the concentration of neuropeptide Y through the vasculature (major arteries and veins), including the renal artery distal to the clip, or in adrenals and brain stem.

Adrenal Glands↗
PubMed1986

Selective renal medullary damage and hypertension in the rat: the role of vasopressin.

The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 +/- 0.6 pg/ml vs 0.8 +/- 0.1 in normal rat, P less than 0.05) but not to pressor levels. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1, receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.

Angiotensin II↗
PubMed1986

Plasma noradrenaline in Goldblatt models of renovascular hypertension in the rat, before and after surgical reversal.

Plasma noradrenaline (NA), blood pressure (BP) and heart rate (HR) were measured simultaneously in conscious rats under basal conditions in the early phase (4-6 weeks) of one-kidney, one-clip hypertension (1K1C), in the early (4-6 weeks) and chronic (greater than 16 weeks) phases of the two-kidney, one-clip model (2K1C) and in age-matched loose clip control animals before and 2 days after unclipping. The elevated BP in all three hypertensive groups fell to normal after unclipping, whereas removal of the constricting clip in loose clip controls had no effect on BP. Plasma NA was elevated in 1K1C hypertension (P less than 0.05) and fell slightly but non-significantly on unclipping. However, in the early phase of 2K1C hypertension plasma NA was unaltered before and rose significantly (P less than 0.05) after unclipping. Plasma NA did not change with unclipping in the chronic phase of 2K1C hypertension and was not different from controls. Unclipping loose clip control animals produced no change in plasma NA. Changes in HR on unclipping followed a similar pattern to changes in plasma NA: changes in the two variables were significantly correlated in all three models (1K1C: r = 0.61, P less than 0.005; early 2K1C: r = 0.45, P less than 0.05; chronic 2K1C: r = 0.62, P less than 0.01). However, BP was only correlated with plasma NA in 1K1C hypertension (r = 0.49, P less than 0.02) and not in either phase of the 2K1C model. There was also a highly significant correlation between HR and plasma NA in 1K1C hypertension (r = 0.71, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

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↗
PubMed1986

Vasodepressor mechanisms in experimental hypertension: studies using chemical medullectomy.

There is evidence that neither activation of the renin-angiotensin system nor changes in sodium balance can fully explain the maintenance of blood pressure in Goldblatt hypertension. Thus, in Goldblatt two-kidney, one clip hypertension in the rat sodium balance is negative and in hypertension of a few months' duration plasma renin initially elevated has returned to normal. When hypertension is reversed by removal of the constricting clip from the renal artery, blood pressure falls within a matter of hours even when hypertension has been present for many months, suggesting that the effect of structural changes in vascular resistance vessels has been overcome. In addition, blockade of the renin-angiotensin system during renal artery declipping does not influence the pattern of the blood pressure fall. We investigated the role of the renomedullary vasodepressor system by inducing medullary necrosis with 2-bromo-ethylamine hydrobromide. This causes a moderate blood pressure increase in normal rats, and partly inhibits the fall of blood pressure in Goldblatt two-kidney, one clip hypertension when the renal clip is removed. Chemical medullectomy is associated with a slightly negative sodium balance, plasma volume contraction, a reduction in plasma renin activity and urinary PGE2, and a minimal elevation in plasma vasopressin. Blood pressure elevation appears to be attributable to inhibition of a vasodepressor system based on the renal medulla. Chemical medullectomy offers a valuable tool for investigating the role of this medullary vasodepressor system.

Animals↗
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↗