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Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions.
Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5·4 ± 0·3 (s.e.m.) to 6·4 ± 0·2 pg/ml) only when plasma angiotensin II levels were supraphysiological.
Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.
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SUMMARY
A radioimmunoassay has been developed for plasma arginine-vasopressin in man and dog. The mean recovery of added arginine-vasopressin (AVP) was 60 ± 6·9 (s.d.)% and the lower threshold of detection 2·0 pmol/l. A close correlation was found between concurrent radioimmunoassay and bioassay values. The mean concentration found in peripheral venous blood in healthy men after overnight fasting was 5·3 pmol/l (range 4·6–6·2 pmol/l). In man, significant increases in plasma AVP occurred after dehydration (5·9–9·5 pmol/l) and significant decreases after oral water-loading (5·2–3·7 pmol/l). During i.v. infusion of graded doses of synthetic AVP in normal men, plasma levels were closely correlated with infusion rate. On stopping the infusion, plasma vasopressin fell exponentially with a half-life of between 7 and 8 min. In man, plasma AVP was unaffected by tilting head-up for 2 h, or by a non-hypotensive bleeding of 500 ml in 10 min. In the dog, haemorrhage of 5 ml/kg and over caused proportionate increases in AVP in the circulation. In normal men, plasma vasopressin was significantly correlated with concurrent urinary osmolality. Five patients with oat-cell bronchial carcinoma and hyponatraemia showed a marked increase of plasma vasopressin. Five patients with diabetes insipidus had significantly reduced, but detectable, levels of plasma AVP. The plasma concentration in these patients did not increase after water restriction.
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Search for other papers by J L Morton in
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Abstract
The mechanisms which initiate and maintain the energy partitioning into maternal tissues during pregnancy are unknown. The present study shows that in each of the weeks prior to pregnancy in the rat, plasma β-cell tropin (βCT) concentrations (nmol/l) were 0·68±0·10, 0·61 ±0·14 and 0·73±0·11 (n=11, mean±s.e.m.). During early (1-3 days) pregnancy the concentration rose to 1·32 ±0·26 and by early-mid (7–10 days) pregnancy they had increased to 1·96 ±0·41. By mid-late (14–17 days) pregnancy plasma βCT concentration had declined to the prepregnancy concentrations (0·67 ± 0·16). This mid-term increase in the circultating concentration of the lipogenic hormone βCT may contribute to the deposition of lipid associated with the early period of gestation. The increased circulating βCT could be derived from the pituitary gland neurointermediate lobe or by secretion from the placenta. It should be emphasised that the measurements in the present study represent a 'snap-shot' at discrete intervals and do not provide information about the dynamic hormonal interplay which occurs physiologically.
Journal of Endocrinology (1995) 146, 177–182
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ABSTRACT
The neurointermediate pituitary peptide β-cell tropin (BCT) has potent insulin-releasing and lipogenic properties and is elevated in obesity and type-2 diabetes. The effects of BCT and glucose on the release of insulin and amylin from the perfused pancreas of obese 'fatty' (fa/fa) rats and lean (Fa/?) controls were measured. Pancreata were perfused, sequentially, with buffer containing: 5·6 mmol glucose/l (basal); basal glucose±0·5 nmol BCT/l; 16·7 mmol glucose/l (high). Insulin and amylin release during basal glucose treatment was eight to nine times greater from pancreata from fatty than from lean rats. BCT induced a fivefold greater monophasic insulin and amylin release from fatty compared with lean pancreata. When not preceded by BCT there was a twofold greater high glucose-induced amylin release from fatty pancreata but no difference in insulin secretion. When preceded by BCT stimulation, high glucose induced twofold greater insulin and fourfold larger amylin release from fatty compared with lean pancreata. Molar secretion ratios of insulin: amylin varied between 30:1 and 50:1. In view of the elevated levels of BCT found in the fatty rat and in the light of the above findings, it is concluded that the peptide may have a role in the development of hyperinsulinaemia, hyperamylinaemia and insulin resistance in this animal model of obesity and diabetes.
Journal of Endocrinology (1993) 137, 375–381
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ABSTRACT
It has been demonstrated that the insulin secretagogue β-cell-trophin, ACTH(22–39), is present in human plasma. The hormone, separated from plasma by affinity chromatography on a corticotrophin-like intermediate-lobe peptide antibody column, behaves similarly to synthetic β-cell-trophin on a gel filtration column and on reverse-phase high-performance liquid chromatography. Sufficient amounts of the hormone were isolated from the plasma of two patients with Nelson's syndrome to demonstrate its biological activity on the perfused rat pancreas.
J. Endocr. (1986) 110, 303–307
