Biomedical subjects
Publications and source records attributed to G Lindop.
Plasma renin levels are elevated in neuroblastoma as in nephroblastoma patients. Unlike nephroblastoma, the active component appears to predominate. Patients with thoracic neuroblastoma produce high levels of renin by the tumour, which thus excludes an ischaemic aetiology as the source.
The adrenocortical tissue which regenerates after adrenal enucleation, and contralateral uninephrectomy and adrenalectomy, resembles histologically zona fasciculata tissue which normally synthesises glucocorticoids. However, increases in blood pressure after enucleation (adrenal regeneration hypertension-ARH] were preceded by a rise in exchangeable body sodium similar to that found with mineralocorticoid-induced hypertension (e.g. DOC/salt rat model). Glucocorticoid involvement in ARH rats was tested, firstly by infusing dexamethasone into control and ARH rats to see whether ACTH suppression would lower blood pressure by reducing adrenocortical activity and, secondly, by infusing dexamethasone into rats with intact adrenals to see whether conditions for ARH (i.e. uninephrectomy and/or saline consumption) pre-disposed rats to the hypertensinogenic properties of glucocorticoids. Low-dose dexamethasone infusions (10 micrograms/day for 5 days) in ARH rats did not affect blood pressure but in control animals caused a significant (P less than 0.01) increase from 128 +/- 3 to 151 +/- 5 mmHg. Corticosterone, 18-hydroxycorticosterone and deoxycorticosterone plasma concentrations were suppressed in both groups by dexamethasone treatment; plasma renin concentrations were lower in ARH rats than in controls. Uninephrectomy or 1% NaCl as drinking fluid did not affect the blood pressure rise induced by sc infusion of 10 micrograms dexamethasone/day for 14 days in rats with intact adrenals. The temporal relationship between blood pressure changes and exchangeable body sodium in ARH rats resembles that in mineralocorticoid-induced hypertension. Glucocorticoid, unlike mineralocorticoid, induced hypertension is not affected by a reduction in renal mass or increased sodium intake.
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Nephrogenic diabetes insipidus associated with high basal levels of plasma arginine vasopressin developed in a patient during lithium therapy. Fluid deprivation was accompanied by an increase in the concentration in peripheral venous plasma of vasopressin and angiotensin II, a rise in plasma osmolality and a modest rise in urine osmolality. Infusion of arginine vasopressin produced comparable levels of plasma vasopressin to those found during fluid deprivation, with no overall change in plasma angiotensin II and little change in urine volume or osmolality. It is suggested that angiotensin II may be responsible for the difference in ability to concentrate urine under these two conditions. Following death by self-poisoning, renal histology revealed distinct structural changes in the distal tubules: such lesions have not previously been described in man and it is suggested that the occurrence of nephrogenic diabetes insipidus while on lithium therapy may be related to tubular damage.
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