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Featured researches published by R. F. Bing.


European Journal of Clinical Pharmacology | 1985

Treatment of essential hypertension: Changes in blood pressure echocardiography and electrocardiography on three therapeutic regimes

G.I Russell; J. E. F. Pohl; J. Baldwin; R. F. Bing; Herbert Thurston; J.D. Swales

SummaryForty-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.


Clinical and Experimental Hypertension | 1982

Vascular Ren in as A Determinant of the Circulatory Response to Renin

M. Loudon; R. F. Bing; J.D. Swales; Herbert Thurston

The effect of an injection of partially purified rat renin on the blood pressure, plasma and aortic renin was studied in rats 18 hours after bilateral nephrectomy. Blood pressure rose and remained elevated 6 hours after renin injection, returning to normal at 9 hours. Aortic renin concentration was increased and showed a similar response pattern to blood pressure whereas plasma renin concentration fell to subnormal levels within 3 hours. The blood pressure response was prevented by converting enzyme inhibition and at 3 and 6 hours was reversed by saralasin infusion. These results demonstrate that circulating renin is taken up by vascular tissue and the pressor response to exogenous renin is related to aortic but not plasma renin.


Archive | 1988

Endogenous Opioids and Reversal of Renovascular Hypertension

M. E. Edmunds; G. I. Russel; R. F. Bing; Herbert Thurston; J.D. Swales

The rapid fall in blood pressure after removal of the constricting clip in two-kidney one-clip hypertension in rats has been well demonstrated [1–3] although the precise mechanism is still not fully understood. Studies on the hemodynamic effects of unclipping suggest that this fall is due to the lowering of total peripheral resistance [4, 5] that occurs while hypertensive structural changes are still present [6], thus implying that vessel tone has become subnormal. Surgical reversal during pharmacological inhibition of the renin-angiotensin system indicated that this pressor mechanism was not fully responsible for the maintenance, or its suppression, of the reversal of this form of hypertension [3]. Sodium retention does not appear to be responsible for the elevated blood pressure [1, 2]. The role of changes in the activity of the sympathetic nervous system in the maintenance of the elevated blood pressure and in its surgical reversal is more controversial [7, 8]. Attention therefore has been directed to possible vasodepressor mechanisms. It is therefore of interest that a recent study has postulated that compounds released in the renal venous effluent after unclipping suppressed tonic efferent sympathetic nervous system activity and also had and effect on behavior, consistent with a central opiate-like action [9]. In other studies, induction of hypertension in the two-kidney one-clip model was associated with altered activity of the endogenous opioid system [10]. Endogenous opioids have been shown to have profound cardiovascular effects in other pathophysiological states [11–13]. In addition to hemodynamic changes invoked by unclipping, cardiovascular effects of any anesthetic used during this procedure will contribute to the initial rapid fall in blood pressure, and therefore obfuscate the true time course of the reversal of hypertension.


The Lancet | 1983

SODIUM TRANSPORT AND HYPERTENSION

Herbert Thurston; R. F. Bing; J.D. Swales


QJM: An International Journal of Medicine | 1987

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

G.I Russell; R. F. Bing; J. A. G. Jones; Herbert Thurston; J.D. Swales


Clinical Science | 1984

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

D. Taverner; R. F. Bing; Fletcher A; G. I. Russell; J.D. Swales; H. Thurston


Clinical Science | 1980

Response of Chronic Renovascular Hypertension to Surgical Correction or Prolonged Blockade of the Renin–Angiotensin System by Two Inhibitors in the Rat

Herbert Thurston; R. F. Bing; E. S. Marks; J.D. Swales


Clinical Science | 1989

Erythrocyte membrane calcium adenosine 5'-triphosphatase activity in the spontaneously hypertensive rat

Abimbola S. Adeoya; Robert I. Norman; R. F. Bing


Clinical Science | 1986

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

G.I Russell; Godfrey Np; Forsling Ml; R. F. Bing; Herbert Thurston; J.D. Swales


Clinical Science | 1981

Haemodynamic changes after surgical reversal of chronic two-kidney, one-clip hypertension in the rat.

G. I. Russell; Brice Jm; R. F. Bing; J.D. Swales; H. Thurston

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J.D. Swales

Leicester Royal Infirmary

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G. I. Russell

Leicester Royal Infirmary

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H. Thurston

University of Leicester

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G.I Russell

Leicester Royal Infirmary

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D. Taverner

University of Leicester

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E. S. Marks

Leicester Royal Infirmary

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Fletcher A

University of Leicester

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