Search PubMed⌕ Search

Biomedical subjects

A F Lever

Publications and source records attributed to A F Lever.

At least 217 records · Page 12Linked to original sources
PubMed1976

Effect of blood pressure angiotensin II and aldosterone concentrations during treatment of severe hypertension with intravenous labetalol: comparison with propranolol.

1 The actions of labetalol 1.0-2.0 mg/kg intravenously on blood pressure, heart rate, plasma angiotensin II and aldosterone concentrations have been studied in 20 recumbent hypertensive patients. 2 In all subjects there was a reduction in systolic and diastolic blood pressures within 5 min of completion of injection. 3 Severe hypotension was not seen but three patients who had a marked fall in blood pressure experienced side-effects. Postural hypotension was common at the end of the study. 4 Labetalol caused significant reduction in heart rate. 5 Labetalol induced significant lowering of plasma angiotensin II and in plasma aldosterone concentrations, which were most obvious when these were increased initially; overall there was a close correlation between concurrent measurements of angiotensin II and aldosterone concentrations. 6 In five patients a comparison was made against propranolol 10 mg intravenously. Labetalol was more effective in lowering blood pressure but less effective in reducing pulse rate of plasma angiotensin II concentration.

Aldosterone↗
PubMed1976

Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism.

The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.

Adenoma↗
PubMed1976

Treatment of phaeochromocytoma and of clonidine withdrawal hypertension with labetalol.

1 Labetalol has been used as medical treatment in five patients with phaeochromocytoma. 2 In four of the five patients, blood pressure was satisfactorily controlled, and symptoms and signs were relieved. 3 Labetalol also provided satisfactory cover across surgery for the removal of tumours in two cases. 4 In one instance, it was not possible to give sufficient labetalol orally to suppress the attacks of phaeochromocytoma. This patient was not effectively controlled at operation with a combination of propranolol and phenoxybenzamine. 5 Intravenous labetalol rapidly lowered blood pressure and relieved symptoms in a patient experienced hypertensive crisis after clonidine withdrawal. 6 Labetalol is a useful addition to the medical treatment of phaeochromocytoma.

Administration, Oral↗
PubMed1975

Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity?

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.

Adult↗
PubMed1975

Results of adrenal surgery in patients with hypertension, aldosterone excess, and low plasma renin concentration.

Fifty patients with hypertension, aldosterone excess, and low plasma renin concentration underwent adrenal surgery. There was a highly significant fall in mean systolic and diastolic pressures after the operation. The mean postoperative diastolic pressure fell to strictly normal levels, however, in only 19 out of 38 patients from whom an adrenocortical adenoma was removed and in only two out of 10 non-tumour patients. There was a significant correlation between the fall in blood pressure during spironolactone treatment and after adrenal surgery though levels were generally slightly lower during the former therapy. It is suggested that removal of an aldosterone-producing adenoma is the treatment of choice provided a good preoperative hypotensive response to spironolactone occurs, while the treatment of choice for non-tumour patients is often long-term spironolactone.

Adenoma↗
PubMed1975

Angiotensin- and norepinephrine-induced myocardial lesions: experimental and clinical studies in rabbits and man.

The ability of large doses of exogenous angiotensin II to cause widespread multifocal microscopic myocardial necrosis in the rabbit has been confirmed. Angiotensin II also consistently produced acute renal failure with, less consistently, renal tubular necrosis. Norepinephrine infusions caused histologically indistinguishable myocardial lesions, but did not detectably affect renal function or histology. Severe renal failure, induced by bilateral nephrectomy (with or without concurrent glycerol administration) was not associated with similar cardiac lesions. Acute renal failure of comparable or greater severity to that induced by angiotensin II was produced by intramuscular cephaloridine, and was not associated with cardiac lesions. Rabbits infused with saline intravenously or "sham"-operated by simply opening and closing the peritoneal cavity did not develop renal failure and showed no cardiac or renal lesions histologically. Myocardial lesions, apparently identical to those seen in the rabbits, were observed postmortem in three patients known to have had high circulating levels of angiotensin II before death, although in all three cases alternative explanations are possible. Unexplained arrhythmia, cardiac arrest, and central chest pain without clear cardiographic or serum enzyme evidence of myocardial infarction occurred in two other subjects with very high plasma levels of angiotensin II. These attacks ceased after bilateral nephrectomy and a consequent fall in plasma angiotensin II. The cardiac attacks in these five patients all occurred during or shortly after procedures, such as sodium-depleting dialysis, renal artery surgery, or diazoxide administration, known to cause increase in plasma concentrations of renin and angiotensin II.

Acute Kidney Injury↗
PubMed1975

Active and passive immunization to angiotensin in experimental acute renal failure.

A number of studies support, and others fail to support, the concept that the renin-angiotensin system plays a key role in the pathogenesis of acute renal failure. This study, employing active and passive immunization against angiotensin II, was designed to examine the primacy of circulating angiotensin as a mediator of this syndrome. Neither mode of immunization significantly affected the degree of azotemia or the marked reduction of inulin clearance expected in rats subjected to glycerol-induced myohemoglobinuria. Twenty-four hours after challenge, inulin clearance (Cin) in actively immunized rats fell to 3.2% of control and that of unimmunized rats given the same dose of glycerol was 2.5% of control. Although there was some variation among groups of passively immunized rats, Cin of one group being 18% of control, Cin of the other groups was less than 3% of control. The dose and binding capacity of the immune globulin used here were essentially the same as those reported in another study in which immunization was thought to be of prophylactic value in rats subjected to s.c. administered glycerol injections. Technologic differences unrelated to immunization are suggested to have caused the difference in results in the two studies, and it seems doubtful that circulating angiotensin plays a key role in the pathogenesis of myohemoglobinuric acute renal failure in the rat.

Acute Kidney Injury↗
PubMed1975

Effect of intravenous frusemide on plasma renin concentration: suppression of response in hypertension.

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.

Adult↗
PubMed1975

Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension.

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.

Adenocarcinoma↗
PubMed1975

Effect of prolonged low-dose angiotensin II infusion on the sensitivity of adrenal cortex in man.

The effect of incremental infusions of isoleucine-5-angiotensin II on blood pressure and plasma aldosterone concentrations was studied in normal man before and after 66 hours of intravenous infusion of angiotensin II at 2 ng kg-1 min-1, sodium and potassium balance being kept roughly constant throughout. Plasma sodium and ACTH concentrations were unaltered, but plasma potassium and magnesium levels and basal plasma cortisol fell slightly after prolonged angiotensin administration. During the prolonged angiotensin infusion plasma renin activity was suppressed, and there was a sustained elevation of arterial pressure and plasma aldosterone concentration. Aldosterone excretion, while clearly increased, showed a regular circadian rhythm, with peak values in the early morning. The angiotensin II-pressor relationship was not significantly changed after the prolonged infusion of angiotensin II, while the angiotensin II-aldosterone dose-response curve was steeper than in the basal state but not identical with that of sodium depletion. No differences were observed in the pressor or aldosterone-stimulant effects of the isoleucine-5 and valine-5 forms of angiotensin II. A trophic effect of angiotensin II on the adrenal cortex may provide a partial explanation for the enhanced response of aldosterone to angiotensin II in sodium depleted man.

Adrenal Cortex↗
PubMed1975

A case of hypopituitarism with diabetes insipidus and loss of thirst. Role of antidiuretic hormone and angiotensin II in the control of urine flow and osmolality.

A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin II (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.

Adult↗