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Biomedical subjects

R F Bing

Publications and source records attributed to R F Bing.

At least 55 records · Page 3Linked to original sources
PubMed1985

Fluid volumes and hemodynamics in hypertension produced by chemical renal medullectomy.

We have investigated the mechanisms by which chemical renal medullectomy with 2-bromoethylamine hydrobromide (200 mg/kg body wt) produces hypertension in rats. Groups of chemically medullectomized rats were compared with normal rats and rats that had been partially nephrectomized to produce an equivalent fall in glomerular filtration rate. Mean arterial pressure was elevated in the medullectomized (142 +/- 6 mmHg) compared with normal rats (124 +/- 3). In the medullectomized animals this was associated with significant tachycardia (483 +/- 15 vs. 450 +/- 6 beats/min) and an increase in cardiac output (61.1 +/- 5.0 vs. 49.9 +/- 2.2 ml X min-1 X 100 g body wt-1). Plasma volume was significantly reduced in medullectomized rats (2.16 +/- 0.15 vs 3.29 +/- 0.20 ml/100 g body wt), whereas exchangeable sodium was unchanged (39.9 +/- 0.5 vs. 39.7 +/- 0.5 meq/kg body wt). By contrast, both plasma volume and exchangeable sodium were increased in partially nephrectomized rats. These results are consistent with the hypothesis that chemical medullectomy produces hypertension by increased selective sympathetic efferent activity, raising cardiac output and postcapillary venular resistance. This may be the consequence of reducing the secretion of a renomedullary humoral substance that normally inhibits such activity.

Animals↗
PubMed1985

Reversal of renovascular hypertension: a comparison of changes in blood pressure, plasma renin, and sodium balance in two models in rats.

Blood pressure changes produced by removal of the renal artery clip in two forms of experimental renovascular hypertension in the rat (two-kidney one-clip and one-kidney one-clip hypertension) have been studied in relation to sodium balance and the renin angiotensin system. Continuous records of arterial blood pressure in conscious, freely moving animals with hypertension of less than 6 weeks' duration showed similar baseline values. After unclipping, blood pressure fell to normal levels within 12 hours of operation, and the pattern of the fall was identical in both models. Plasma renin concentration was elevated in two-kidney hypertension and fell to normal by 24 hours after operation, remaining unchanged 6 days later, whereas in one-kidney hypertension it was normal before and after unclipping. Sodium balance became positive in two-kidney hypertension within 24 hours of unclipping and remained so at 7 days, and was significantly different from that in unclipped loose-clip controls (+2.54 +/- 0.55 mmol vs. +0.46 +/- 0.55 mmol at 7 days, P less than 0.05). In one-kidney hypertension, sodium balance was negative during the first 24 hours after operation, and remained slightly negative at 7 days compared with loose-clip controls (-0.34 +/- 0.23 mmol). The similarity in the pattern of blood pressure fall in these two models of renovascular hypertension, despite qualitative differences in the response of sodium balance and the renin-angiotensin system, suggests that a common mechanism is activated by unclipping. This mechanism cannot be explained solely in terms of changes in sodium balance or activity of the renin-angiotensin system.

Animals↗
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↗
PubMed1984

The effect of ageing on the response to frusemide in normal subjects.

The effect of IV frusemide was studied in six healthy young (mean age 26.5 years, range 21-33) and six healthy old (mean age 72.8 years, range 66-80) volunteers. A 24-h urine collection before frusemide showed no difference in volume and sodium excretion, although the old excreted less potassium. Creatinine clearance was significantly reduced in the older subjects. After frusemide, 20 mg IV, the pattern of sodium and water excretion over a 5-h period was different in the two groups. The peak effect was greater in the young and occurred within the first 30 min, but was delayed to between 30 and 60 min in the old. Thus in the young the time for 50% of the total sodium and water to be excreted was half that in the old. This delay in sodium and water excretion was related to baseline creatinine clearance. However, the total water, sodium and potassium excreted in the 5 h after frusemide did not differ in the two groups. These results suggest that the renal effects of frusemide are different in healthy elderly subjects as compared to the young. The delayed and reduced peak response is consistent with fewer nephrons in the elderly kidney.

Adult↗
PubMed1984

Effect of unclipping on pressor responses in rats with renovascular hypertension.

Pressor responses to angiotensin II and noradrenaline have been examined in two models of renovascular hypertension (two-kidney one-clip and one-kidney one-clip) before and 24 h after removal of the renal artery clip to examine the possible role of pressor hyper-responsiveness in the maintenance of hypertension. Early and chronic hypertension was studied to assess the part played by progressive structural hypertrophy. Plasma renin concentration was elevated in early two-kidney hypertensive rats, whereas it was similar to that in age-matched normal rats in early one-kidney and chronic two-kidney hypertensive rats. Twenty-four hours after unclipping plasma renin concentration was the same in all groups. Unclipping restored blood pressure to normal levels by 24 h, whereas sham-operated animals remained hypertensive. Angiotensin II responses in both early and chronic two-kidney one-clip hypertensive rats were lower than in age-matched normal rats. In unclipped rats responses were similar to those in normals. One-kidney hypertensive rats had similar angiotensin II responses to normal rats and there was no change with unclipping. Blockade of endogenous angiotensin II production by converting enzyme inhibition resulted in similar angiotensin II responses in hypertensive and unclipped groups. In normal rats, angiotensin II responses were inversely related to plasma renin concentration (r = -0.47, P less than 0.001). Angiotensin II responses in hypertensive and unclipped rats were found to show a similar relationship to plasma renin concentration as normal rats. Noradrenaline responses in hypertensive rats were similar to those in age-matched normals and there was no significant change with unclipping.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1984

Hypertension produced by chemical renal medullectomy: evidence for a renomedullary vasodepressor function in the rat.

The rat renal papilla was selectively destroyed by 2-bromoethylamine hydrobromide; increasing doses produced a graded severity of histological damage, polyuria and a reduction in urinary prostaglandin E2 excretion. Destruction of at least half of the papilla caused significant hypertension, but plasma renin concentration and plasma creatinine did not change. After graded medullary damage Goldblatt two-kidney, one-clip hypertension was induced. Four weeks later the severity of hypertension was similar in medulla-damaged and medulla-intact groups. When Goldblatt two-kidney, one-clip hypertension was reversed by removal of the renal artery clip, the blood pressure fall was less when the inner renal papilla was ablated than when it was intact, although plasma renin concentration and sodium balance were similar. The final blood pressure was similar to that observed in normal rats treated with 2-bromoethylamine compared with their respective controls. These findings are consistent with the hypothesis that the inner renal medulla produces a vasodepressor that influences blood pressure in normal rats, and also lowers blood pressure when two-kidney, one-clip hypertension is reversed surgically.

Animals↗
PubMed1984

Cell membrane handling of sodium, sodium balance, and blood pressure.

A variety of abnormalities in cell membrane cation handling have been reported in hypertension. It is not known whether abnormal transport serves as a marker of an underlying disturbance in cell membrane function or whether one or more of the abnormal transport processes participate directly in the sequence of events that cause hypertension. One critical area is the response of membrane sodium transport to salt depletion and loading. To elucidate a possible relationship between changes in sodium balance, membrane cation transport, and blood pressure, we studied the effect of salt depletion and loading in two cells from two separate species--the rat thymocyte and the human white blood cell. In each, severe salt depletion significantly reduced ouabain-sensitive sodium efflux, while salt loading produced a non-significant increase. No significant changes in the sodium efflux rate constant were observed in thymocytes from Okamoto-Kyoto spontaneously hypertensive rats or from rats with Goldblatt one-kidney, one-clip or deoxycorticosterone-salt hypertension when they were compared with appropriate controls. However, both Okamoto-Kyoto hypertensive rats and Kyoto controls showed a highly significant fall in the sodium efflux rate constant with age. These findings indicate that the reduction in sodium pumping observed in hypertensive human patients is not attributable directly or indirectly to salt excess, since in the two species studied reduced sodium pumping was a physiological response to salt depletion. Further, altered membrane transport of sodium may reflect factors that affect cell composition (such as age) rather than participate directly in the pathogenesis of hypertension.

Animals↗
PubMed1984

Diuretics, sodium intake, and renin in the management of hypertension.

Twenty-four-hour urinary sodium excretion and plasma renin activity were monitored in 36 patients receiving bendrofluazide as sole antihypertensive therapy. There was no increase in urinary sodium output compared with pretreatment values during a 2-year period, and there is therefore no evidence that an increase in salt appetite as a result of salt depletion occurred. However, plasma renin activity progressively increased over a 2-year period. In five of eight patients who initially had a subnormal renin response to the diuretic, plasma renin level rose into the normal stimulated range. When administration of the diuretic was stopped in 10 patients after a mean treatment period of 49 months, plasma renin activity promptly fell and weight increased significantly, although blood pressure did not rise. However, on rechallenging with bendrofluazide 28 days later, a greater response was observed than when treatment was originally instituted. Further, three of five patients with low renin hypertension had a normal response on the second occasion. Thus prolonged diuretic therapy has a persistent effect on the activity of the renin-angiotensin system as well as on blood pressure for at least 4 weeks after the discontinuation of diuretics.

Adult↗
PubMed1984

Delayed reversal of Goldblatt hypertension by angiotensin II infusion in the rat.

Reversal of early Goldblatt two-kidney, one-clip hypertension is associated with a fall in plasma renin. To define the role of this in blood pressure normalization we maintained preoperative hypertension for 12 h after unclipping or removal of the ischemic kidney, by angiotensin II or norepinephrine infusions during continuous blood pressure monitoring. High infusion rates of angiotensin II (1 microgram X kg-1 X min-1) were needed to reproduce hypertensive pressures. On stopping angiotensin II there was a rapid initial fall in blood pressure but not to normal (176 +/- 3.1 to 138 +/- 4.3 mmHg at 1 h), and a later slower fall to normal by 24 h (114 +/- 3.9). This response was identical to that of dextrose-infused animals (180 +/- 8.2 to 146 +/- 7.0 at 1 h and 113 +/- 5.6 at 24 h), apart from a transient rise in blood pressure associated with hyperreninemia in unclipped animals 12 h postinfusion. In contrast, after norepinephrine blood pressure fell immediately to normal. Similar responses were seen in normal rats after 12-h pressor infusions of angiotensin II or norepinephrine. These results show that the fast and slow components of the blood pressure fall following reversal of Goldblatt hypertension are delayed but otherwise unaltered specifically by angiotensin II. The need for pharmacologic doses, however, suggests that mechanisms in addition to the direct vasopressor action of angiotensin II are involved.

Angiotensin II↗
PubMed1984

Hypertension produced by chemical renal medullectomy or partial nephrectomy in the rat: comparison of renal function and plasma volume.

Glomerular filtration rate, plasma volume and intra-arterial blood pressure were measured in conscious rats, with hypertension induced by chemical medullectomy or partial nephrectomy and compared with those in sham treated normal rats. Both medullectomy and partial nephrectomy caused a similar rise in blood pressure. Hypertension produced by partial nephrectomy was associated with plasma volume expansion but after chemical medullectomy there was a marked hypovolaemia. These results suggest that volume expansion plays no part in chemical medullectomy hypertension but are in keeping with the hypothesis that the renal medulla releases a vasodepressor substance which plays an important role in the maintenance of normal blood pressure.

Animals↗
PubMed1983

Calcium antagonists in hypertension: relation to abnormal sodium transport.

Leucocyte sodium efflux rate constants and intracellular electrolyte contents were estimated in 13 patients with untreated essential hypertension. There was no correlation between intracellular sodium or potassium content or efflux rate constant and blood pressure. The patients were then treated with oral nifedipine and blood pressure controlled. Sodium efflux rate constants and electrolyte contents were estimated one and three months after the start of treatment. There was a significant fall in blood pressure, but mean sodium efflux rate constant and intracellular sodium content were unchanged. There was no correlation between the fall in blood pressure, initial sodium efflux, or intracellular sodium content. These data do not support the hypothesis that the sodium pump and intracellular sodium content have a direct role in generating raised blood pressure, or that treatment of hypertension with calcium antagonists corrects a fundamental alteration of calcium-sodium exchange across the cell membrane.

Blood Pressure↗