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Biomedical subjects

R F Bing

Publications and source records attributed to R F Bing.

At least 73 records · Page 4Linked to original sources
PubMed1983

Surgical reversal of renovascular hypertension in rats: changes in blood pressure, plasma and aortic renin.

1. Blood pressure, plasma and aortic renin concentrations were measured in Goldblatt two-kidney one-clip hypertensive rats before and after surgical correction by removing the renal artery clip. 2. Blood pressure fell rapidly in the first hour and then more slowly over 24 h. 3. Plasma renin concentration fell into the normal range by 3 h after unclipping. 4. Aortic renin concentration was markedly raised in hypertensive rats and declined slowly after unclipping, being virtually unchanged at 3 h and reaching normal levels at 24 h. 5. The fall in blood pressure produced by removal of the renal artery clip in Goldblatt two-kidney one-clip hypertensive rats does not depend upon the renin-angiotensin system in plasma and vascular tissue and indicates that a renal vasodepressor system may be involved.

Animals↗
PubMed1983

Hemodynamic changes induced by reversal of early and late renovascular hypertension.

The hemodynamic changes associated with reversal of Goldblatt two-kidney, one-clip hypertension in conscious rats were studied using radioactive microspheres. In both the early phase (less than 6 wk from clipping) when plasma renin was elevated and the chronic phase (greater than 4 mo) when plasma renin was normal, hypertension was maintained by elevated peripheral resistance. Unclipping or removal of the ischemic kidney normalized blood pressure within 24 h by reduction in peripheral resistance. In early-phase hypertension blood pressure remained normal at 60 days after nephrectomy or unclipping, but in chronic-phase hypertension blood pressure was significantly elevated at 60 days after nephrectomy despite a similar fall in peripheral resistance. Plasma renin fell to normal or subnormal values after reversal in both early and chronic hypertension. Thus reversal of hypertension is associated with a rapid reduction in peripheral resistance even in longstanding hypertension. Since removal of the ischemic kidney and unclipping were equally effective, reversal must depend on either inhibition of a pressor system derived from the ischemic kidney or activation of a peripheral vasodepressor system not dependent on a revascularized kidney.

Acute Disease↗
PubMed1983

Renin in the arterial wall.

Homogenates of rat aortic wall can generate angiotensin I when incubated with nephrectomised rat plasma. This renin-like activity is due to a mixture of proteolytic enzymes. Thus the capacity to generate angiotensin I is greater at pH 5.3 than pH 6.5, although the latter is the pH optimum for rat renal renin. The present work addresses itself to two questions. Is this activity derived from plasma renin? Secondly, does vascular renin-like activity play a role in blood pressure control? Plasma and aortic renin were altered by bilateral nephrectomy and modulation of salt intake. In addition four models of hypertension were studied (early and chronic Goldblatt 2-kidney 1-clip, DOC-salt and spontaneous hypertension). The results indicated that in steady state conditions, aortic and plasma renin-like activity (measured with an incubation pH of 6.5) changed in parallel. When plasma renin was altered acutely however by intravenous injection of renin into nephrectomised rats the half-life of plasma renin was much shorter than the half life of aortic renin. Under these circumstances the pressor response to renin correlated much better with aortic than with plasma renin-like activity. Whilst these studies suggest therefore that renin taken up by the arterial wall is an important determinant of blood pressure, they provide no evidence that accumulation of renin locally produces hypertension in the presence of normal or low plasma renin activity.

Animals↗
PubMed1983

Arterial wall renin.

Aortic homogenates contain proteolytic enzymes which will release angiotensin I (AI) from renin substrate. Some of these are active at low pH and are probably unrelated to renin. Renin-like activity in the rat measured at the optimum pH of 6.5 is altered in parallel with plasma renin in a wide variety of situations. The two diverge only in non-steady state situations. Studies have therefore been carried out after bilateral nephrectomy and after the injection of renal renin into nephrectomized rats. In each case aortic renin-like activity was cleared much more slowly than plasma renin, and the blood pressure change was related to aortic renin-like activity rather than to plasma renin. The blood pressure response to the converting enzyme inhibitor teprotide was also related to the former rather than the latter. Immunofluorescent studies of the aorta and the intrasplenic arteries from rats injected with mouse renin showed that renin was taken up predominantly into the media and persisted at this site. Thus, the uptake of renal renin from plasma by both large and small arteries is probably an important step in the physiology of the renin-angiotensin system and mediates renin-induced changes in peripheral resistance and blood pressure. However, we have no evidence for the hypothesis that selective accumulation of renin in the resistance vessel walls causes hypertension when circulating levels of renin are normal.

Animals↗
PubMed1983

Chemical renal medullectomy and experimental hypertension.

The possible vasodepressor role of the renal medulla was studied by chemical medullectomy (i.v. bromoethylamine hydrobromide) in rats. A significant increase in blood pressure (BP) was observed 10 weeks after injection which related to the increase in urinary volume and decrease in urinary prostaglandin E2 (PGE2) in medullectomised rats, but not to plasma renin concentration (PRC). Creatinine clearance was unchanged. The differences between control and medullary damaged rats were maintained over a wide range of sodium intakes although the patterns of response were similar in the two groups. The increase in BP observed following renal medullectomy is likely to be secondary to a reduction in interstitial cell function.

Animals↗
PubMed1983

Chemical renal medullectomy: effect on blood pressure in normal rats.

The renal medulla may have a vasodepressor function in blood pressure control. We have studied the effect of selective ablation of the medulla produced with 2-bromoethylamine hydrobromide on blood pressure in the rat. Increasing doses of bromoethylamine produced a corresponding degree of histological damage. Five weeks after medullary ablation intra-arterial blood pressure was elevated only in those groups of animals which had confluent necrosis of the papilla. The degree of hypertension was not related to plasma renin concentration but showed a significant correlation with urinary prostaglandin E2 excretion. Hypertension in medullectomized animals is probably due to a loss of a medullary vasodepressor function.

Animals↗
PubMed1983

The role of vascular hypertrophy in early and chronic renovascular hypertension.

Pressor responsiveness to angiotensin II and noradrenaline have been examined using a blood perfused hind limb preparation in early and chronic renovascular hypertension before and after correction of the hypertension by removing the renal artery clip. Hypersensitivity was only partially developed in the early phase but markedly so in the chronic phase. After renal artery unclipping blood pressure returned to normal within 24 h despite the continued presence of enhanced vascular reactivity. When studied 60 days after unclipping, pressor responsiveness had returned to normal in both previously early and chronic hypertensive rats. These results suggest that hypersensitivity to pressor agents develops after hypertension has become established and as a consequence of structural vascular change in response to the raised blood pressure. Although these changes may play a role in the maintenance of blood pressure in chronic hypertension they are of little importance in the development of hypertension.

Acute Disease↗
PubMed1983

Improvement of renal function during long-term treatment of severe hypertension with minoxidil.

Sixty-nine patients with refractory hypertension were treated with minoxidil and in 66 good control of blood pressure was achieved. Renal function was stabilized in 31 patients in whom the serum creatinine was normal at presentation. Twenty-eight patients with impaired renal function had a substantial fall in serum creatinine (25 per cent) during the first three to six months of treatment and this improvement was maintained. In contrast, renal function in six out of seven patients with primary renal disease continued to deteriorate despite adequate control of blood pressure. Effective control of blood pressure prevents or reverses impairment of renal function in patients with refractory hypertension not associated with primary renal disease.

Blood Pressure↗
PubMed1982

Leucocyte membrane sodium transport in normotensive populations: dissociation of abnormalities of sodium efflux from raised blood-pressure.

Sodium efflux rates were measured in leucocytes from eighteen normotensive subjects who had one or more first-degree relatives with essential hypertension and from twenty-four matched controls with no such family history. The total efflux rate constant was significantly lower in those with a family history of hypertension, owing to reduced ouabain-sensitive sodium pump activity. The presence of a membrane electrolyte handling abnormality characteristic of essential hypertension in normotensive individuals genetically predisposed to hypertension points to an underlying genetic factor. At the same time, the fact that blood-pressure was normal in these subjects indicates that the abnormality does not participate directly in blood-pressure elevation. Rather, the abnormality, like other red-cell changes in electrolyte handling, seems to be a marker for a genetically determined alteration in membrane structure, and thus only indirectly related to hypertension.

Adult↗
PubMed1982

Treatment of refractory hypertension.

126 patients with blood pressure which was unacceptably high despite a conventional stepped-care regimen (diuretic, beta-blocker, and vasodilator) took part in a comparative assessment of different approaches to the treatment of refractory hypertension. One of four regimens was used: oral diazoxide, minoxidil, captopril, or quadruple therapy (diuretic + beta-adrenoceptor blocker + hydralazine + prazosin). Despite the severity of hypertension, blood pressure could be controlled in almost all these patients, and no patient died from cerebrovascular disease while on treatment. 2 patients died of renal failure and 5 patients required long-term haemodialysis. Ischaemic heart disease remained a problem and caused the death of 10 patients. Diazoxide was the most effective treatment but was the most difficult and unpleasant to use. Captopril was the best-tolerated but failed to control blood pressure in 6 of 15 patients. Our experience indicates that there are now sufficient therapeutic alternatives to achieve acceptable blood-pressure control in almost all patients with "refractory" hypertension, although no treatment is ideal.

Adrenergic beta-Antagonists↗
PubMed1982

Indomethacin or aprotinin infusion: effect on reversal of chronic two-kidney, one-clip hypertension in the conscious rat.

1. Blood pressure was monitored continuously in conscious rats with chronic Goldblatt two-kidney, one-clip hypertension. 2. Hypertension was rapidly reversed by removal of the constricting clip and the reversal was complete by 12 h, although structural vascular changes persisted for much longer. 3. Blood pressure in this model of hypertension was not affected by a 15 h infusion of either indomethacin or aprotinin. 4. The pattern of fall in blood pressure after removal of the clip was similar when animals were infused with either indomethacin or aprotinin. Blood pressure at 24 h was normal and did not differ significantly from that of unclipped rats given a glucose infusion. 5. The fall in blood pressure produced by unclipping therefore did not appear to be mediated via the prostaglandin or kallikrein systems.

Animals↗
PubMed1982

Plasma renin in long-term diuretic treatment of hypertension: effect of discontinuation and restarting therapy.

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular 'low renin hypertension' may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

Bendroflumethiazide↗
PubMed1982

The addition of prazosin to standard triple therapy in the treatment of severe hypertension.

1 A small dose of prazosin was added to the treatment regime of sixteen hypertensive patients poorly controlled on a combination of bendrofluazide, hydralazine and propranolol. 2 There was a significant improvement in blood pressure control in all patients at 1 month (P less than 0.01) and this was maintained at 9 months (P less than 0.02). Tolerance to prazosin was not a problem. 3 The addition of prazosin to conventional triple drug therapy produces a further useful fall in blood pressure.

Adult↗
PubMed1982

Effect of sodium, deoxycorticosterone and duration of hypertension on pressor responses in rats.

1. Enhanced pressor responsiveness to angiotensin II and noradrenaline has been demonstrated in the hypertension that follows deoxycorticosterone (DOC) and salt administration in the rat. The present studies were carried out to assess the importance of factors common to both pressor agents and those specific to individual agents such as receptor availability.2. Accordingly pressor reponses to angiotensin II and noradrenaline have been studied in normotensive salt-loaded and sodium depleted rats with and without DOC, and in rats with DOC-salt hypertension of short and long duration. These responses have been related to the plasma renin levels in the animals studied.3. Pressor reponses to angiotensin II were increased, dose-response curve (d.r.c.) shifted to the left, in salt-loaded rats and the administration of DOC produced a further increase. DOC-salt hypertension of short duration was associated with an even greater responsiveness. Sodium depletion, however, reduced responsiveness (d.r.c. shifted to the right) and concurrent DOC administration did not alter this. Angiotensin II responses were closely correlated with plasma renin concentration over a wide range of values (p.r.c, r = -0.77, P < 0.001). The differences between the groups could be explained therefore by the number of unoccupied angiotensin II receptors available.4. On the other hand only sodium loaded rats that were also receiving DOC showed any change in noradrenaline responsiveness, when the dose-response curve was shifted to the left. Noradrenaline responses showed no linear relationship to plasma renin concentration.5. The presence of hypertension did not significantly alter noradrenaline responses and the increase observed in angiotensin II responsiveness could be explained by the greater suppression of plasma renin in this group. Duration of hypertension had no effect on responsiveness to either agent.6. These results point to important differences in the pressor responsiveness to angiotensin II and noradrenaline with variation of salt intake and DOC administration.

Angiotensin II↗
PubMed1982

Early remission in thyrotoxicosis produced by short courses of treatment.

Twenty-eight patients with Graves' disease were treated with short-term antithyroid drug therapy. i.e. treatment was discontinued as soon as they became euthyroid. This was less than 4 months in all patients. Ten patients remained euthyroid, although in two of these, thyrotoxicosis recurred after the patients had been euthyroid for more than 2 months. The other 18 patients relapsed within 12 weeks of stopping therapy, and only two have become euthyroid after a further 12 month period of treatment. All patients who remitted were thyrotoxic for the first time whereas all patients with a past history of thyroid disease relapsed. Positive thyroid microsomal antibody titres were more frequent in patients who remitted, otherwise there were no indicators of a favourable outcome. The remission rate with antithyroid therapy which is only continued until the patient becomes euthyroid is similar to that for treatment lasting 12--18 months. Short-term therapy has the advantage of savings in both patient and clinician time.

Carbimazole↗
PubMed1982

Vascular renin as a determinant of the circulatory response to renin.

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.

Animals↗