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Biomedical subjects

B Leckie

Publications and source records attributed to B Leckie.

At least 37 records · Page 2Linked to original sources
PubMed1983

An ultrastructural and immunocytochemical study of a renal carcinoma secreting inactive renin.

This is a case report of a renal carcinoma which was secreting inactive renin. Using an antibody to human renin and the indirect immunoperoxidase technique, the renin-containing cells were localised within the tumour. These were found to be small granular cells situated in a perivascular position. The histological immunocytochemical and ultrastructural features of these cells are described.

Adenocarcinoma↗
PubMed1983

Peptide inhibitors of renin.

Three experiments are described using new substrate analogue inhibitors of renin. The first experiment shows that introduction of a reduced isostere in the scissile peptide bond of an analogue greatly increases its ability to inhibit renin of a particular species. However, different species of renin substrate have different amino acids in their scissile bond and variation here also greatly influences the affinity of renin and substrate and hence of renin and substrate analogues. Finally, substitution of amino acids in the C-terminal adjacent to the scissile bond influences the affinity and efficacy of substrate analogues as inhibitors. In our second experiment a peptide inhibitor of dog renin, H.77, was used in an affinity column to produce a one-stage, 2000-fold, and complete purification of human renin. In our third experiment infusion of H.77 was used to lower circulating concentrations of angiotensin I and angiotensin II in conscious sodium-deplete dogs. Captopril was then given in addition to H.77 but blood pressure did not fall further, suggesting that captopril lowers blood pressure wholly or partly by reducing angiotensin II within the circulation and in extravascular sites.

Amino Acid Sequence↗
PubMed1982

Captopril treatment: inter-dose variations in renin, angiotensins I and II, aldosterone and blood pressure.

1 The ability of captopril, 150 mg three times daily by mouth, to effect sustained reduction in plasma angiotensin II, with converse increases in circulating angiotensin I, and in active, inactive and total renin concentrations, has been assessed. 2 During prolonged treatment with captopril alone, and 12 h after the last dose of the drug, plasma angiotensin II remained approximately one-sixth of basal concentrations, while angiotensin I and renin concentrations were proportionately increased. However, further increases in angiotensin I, and in active, inactive and total renin concentrations, were seen 2 and 6 h after the morning dose of 150 mg captopril. 3 Inter-dose variations in plasma aldosterone and blood pressure were not closely related to concurrent variations in the renin-angiotensin system. 4 Arguments are presented for relying on measurements of plasma renin and angiotensin concentrations rather than of renin activity or aldosterone in assessing the effectiveness of converting enzyme inhibition.

Adolescent↗
PubMed1980

Captopril in clinical hypertension. Changes in components of renin-angiotensin system and in body composition in relation to fall in blood pressure with a note on measurement of angiotensin II during converting enzyme inhibition.

The effect of the converting enzyme inhibitor captopril on arterial pressure, the components of the renin-angiotensin-aldosterone system, and body sodium and potassium content was studied in eight hypertensive patients with renal artery stenosis and, in conjunction with diuretics, in seven patients with hypertension unresponsive to previous treatment. Two hours after the first dose, captopril caused significant falls in systolic and diastolic pressures, plasma angiotensin II, and aldosterone, with converse increases in angiotensin I and both active and total renin; the initial fall in diastolic pressure was significantly related to the drop in plasma angiotensin II. The biochemical changes were sustained during prolonged treatment, even when diuretics were added. One untreated patient with renal artery occlusion had severe secondary aldosterone excess, was sodium and potassium depleted, and severely hyponatraemic and hypokalaemic; captopril restored blood pressure, plasma electrolyte concentrations, and exchangeable sodium and total body potassium to normal. In one man with renal artery stenosis and overall renal impairment captopril led to sodium retention, and blood pressure did not fall until a diuretic was added. In the remaining patients with renal artery stenosis, pretreatment renin, angio tensin II, and aldosterone concentrations were either normal or only modestly raised, and plasma electrolyte concentrations and body content of sodium and potassium were normal. Captopril alone controlled arterial pressure in all, three cases showing a gradual fall of pressure over the first six weeks of treatment; no significant changes in exchangeable sodium or total body potassium were seen. The group of patients with previously intractable hypertension were all controlled with a combination of captopril and diuretic.

Aldosterone↗
PubMed1979

T and B lymphocytes in patients with acute anterior uveitis and ankylosing spondylitis, and in their household contacts.

During episodes of acute anterior uveitis, patients had a T-lymphopenia and a temporary increase in B-lymphocytes. The T-lymphopenia was not present in patients investigated early in their first attacks, and it persisted after the patients recovered clinically. In household contacts of patients with uveitis, there was a temporary T-lymphopenia. A similar degree of T-lymphopenia was present in patients with ankylosing spondylitis who had not had uveitis, but not in their household contacts. In patients with spondylitis, there was no greater reduction of T-cells when they had episodes of uveitis. In all groups of subjects studied, T-lymphopenia could be abolished, in vitro, with thymosin, a bovine thymic-hormone estract. The finding of T-lymphocyte depletion in the contacts of uveitis patients, as well as in the patients themselves, suggests that there may be lateral transmission of an infective agent (or agents) in the households during (or before) attacks of uveitis.

Acute Disease↗
PubMed1979

Hyponatraemic hypertensive syndrome with renal-artery occlusion corrected by captopril.

Malignant hypertension with severe hyponatraemia, hypokalaemia, depletion of sodium and potassium, and elevated blood levels of renin, angiotensin I, angiotensin II, aldosterone, and arginine vasopressin developed in a woman with renal-artery occlusion. Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Captopril, by inhibiting conversion of angiotensin I to angiotensin II, further elevated the blood levels of renin and angiotensin I but corrected all other abnormalities. Unilateral nephrectomy was subsequently curative.

Aldosterone↗
PubMed1978

A renal carcinoma secreting inactive renin.

1. A patient presented with mild hypertension, a raised plasma total renin concentration but a normal plasma angiotensin II concentration. The discrepancy was due to a high concentration of inactive renin in the plasma. 2. A renal carcinoma was detected and removed. The tumour contained a higher proportion of inactive renin than was found in uninvolved areas of the kidney. After unilateral nephrectomy, the plasma concentration of inactive renin fell to normal. 3. Six months later, plasma inactive renin concentration again increased and a metastasis was detected in a rib. Excision of the rib together with radiotherapy resulted in a fall in plasma inactive renin to normal. 4. The inactive renin in plasma and tumour extracts was activated to the same extent by acid treatment and by trypsin.

Aged↗