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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin hypoglycaemia causes a rise in plasma vasopressin concentrations in man and the rat, and vasopressin stimulates glucagon secretion and increases hepatic glucose output in man. Vasopressin has also been suggested to have an important synergistic role with corticotrophin releasing factor in the release of adrenocorticotrophin hormone, and a counter-regulatory role for the hormone has been proposed. As diminished anterior pituitary hormone responses to hypoglycaemia have been reported in diabetes mellitus, we studied the plasma vasopressin responses to insulin-induced hypoglycaemia in 10 patients with established Type 1 diabetes and 10 matched control subjects. Blood glucose fell from 4.5 +/- 0.3 to 1.6 +/- 0.1 mmol l-1 (p less than 0.001) in the diabetic group and from 4.6 +/- 0.2 to 1.5 +/- 0.2 mmol l-1 (p less than 0.001) in control subjects, with delayed blood glucose recovery in the diabetic patients. Plasma vasopressin rose in the diabetic patients from 0.9 +/- 0.2 to 6.9 +/- 2.8 pmol l-1 (p less than 0.001), a significantly greater rise (p less than 0.05) than in the control subjects, 0.8 +/- 0.1 to 2.4 +/- 1.0 pmol l-1 (p less than 0.001). Plasma osmolalities remained unchanged and haemodynamic changes were similar in both groups. There is an exaggerated rise in plasma vasopressin concentrations in diabetic patients in response to insulin-induced hypoglycaemia. The putative mechanisms and potential significance of the exaggerated rise are discussed.
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PMID:Vasopressin secretion during insulin-induced hypoglycaemia: exaggerated responses in people with type 1 diabetes. 252 60

The diabetes insipidus which accompanies the DIDMOAD (Wolfram) syndrome is thought to be hypothalamic in origin, though no formal study of vasopressin secretion in the syndrome has been published, and some data in the literature suggest a renal tubular defect. We have studied vasopressin secretion in seven patients with the Wolfram/DIDMOAD syndrome during three dynamic stimuli: an osmotic stimulus (hypertonic saline infusion), hypoglycaemia (insulin tolerance test) and a baroregulatory stimulus (trimetaphan infusion). Hypertonic saline infusion demonstrated three patients to have complete and four to have partial hypothalamic diabetes insipidus; administration of (per nasal) desmopressin excluded nephrogenic diabetes insipidus in all seven patients. Insulin hypoglycaemia failed to stimulate vasopressin release, but trimetaphan-induced hypotension produced significant though subnormal rises in plasma vasopressin in three patients with partial diabetes insipidus, though it produced a negligible rise and no rise in plasma vasopressin in two patients with complete diabetes insipidus. The data suggest a much greater frequency of hypothalamic diabetes insipidus in the Wolfram/DIDMOAD syndrome than is reported, but did not identify nephrogenic diabetes insipidus. The absence of vasopressin responses to non-osmotic stimuli in patients with complete diabetes insipidus suggests global lack of vasopressin secreting neurones, rather than an isolated osmoreceptor defect or selective vasopressin secreting neuronal loss, as the lesion producing diabetes insipidus in the DIDMOAD syndrome.
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PMID:Vasopressin secretion in the DIDMOAD (Wolfram) syndrome. 268 31

Plasma corticotrophin (ACTH) and corticosteroid levels in response to lysine vasopressin (LVP), insulin hypoglycaemia, and pyrogen have been compared in seven subjects with normal pituitary adrenal function. Intramuscular vasopressin was a weak stimulus to corticotrophin release, peak values lying within the range 49 to 141 pg/ml. Insulin hypoglycaemia consistently caused a more noticeable increase, with peak levels between 114 and 364 pg/ml, while pyrogen was the most powerful, corticotrophin levels rising to between 209 and 1,725 pg/ml. Peak plasma corticosteroid levels showed less pronounced differences between the three tests, and correlated poorly with peak ACTH levels. Thus, relatively small acute changes in corticotrophin levels produce near-maximal adrenal stimulation. Under these conditions, plasma corticosteroid measurements do not accurately reflect circulating corticotrophin levels. These findings help to explain the physiological basis of several observations on the corticosteroid responses to these clinical test procedures.
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PMID:Comparison of corticotrophin and corticosteroid response to lysine vasopressin, insulin, and pyrogen in man. 434 79