R. F. Bing
Leicester Royal Infirmary
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Featured researches published by R. F. Bing.
European Journal of Clinical Pharmacology | 1985
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
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
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
Herbert Thurston; R. F. Bing; J.D. Swales
QJM: An International Journal of Medicine | 1987
G.I Russell; R. F. Bing; J. A. G. Jones; Herbert Thurston; J.D. Swales
Clinical Science | 1984
D. Taverner; R. F. Bing; Fletcher A; G. I. Russell; J.D. Swales; H. Thurston
Clinical Science | 1980
Herbert Thurston; R. F. Bing; E. S. Marks; J.D. Swales
Clinical Science | 1989
Abimbola S. Adeoya; Robert I. Norman; R. F. Bing
Clinical Science | 1986
G.I Russell; Godfrey Np; Forsling Ml; R. F. Bing; Herbert Thurston; J.D. Swales
Clinical Science | 1981
G. I. Russell; Brice Jm; R. F. Bing; J.D. Swales; H. Thurston