NDLI: Vasopressin function in familial cranial diabetes insipidus.

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Vasopressin function in familial cranial diabetes insipidus.

Content Provider	Semantic Scholar
Author	Baylis, Peter H. Robertson, Gary L.
Copyright Year	1981
Abstract	A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.
Starting Page	36
Ending Page	40
Page Count	5
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://pmj.bmj.com/content/postgradmedj/57/663/36.full.pdf
PubMed reference number	7279821v1
Volume Number	57
Issue Number	663
Journal	Postgraduate medical journal
Language	English
Access Restriction	Open
Subject Keyword	Apomorphine Argipressin Autosomal dominant inheritance Central Diabetes Insipidus Hypoglycemia Nausea Patients Polyuria Saline Solution, Hypertonic Thirst Trimethaphan Vasopressins Water-Electrolyte Balance vasopressin secretion
Content Type	Text
Resource Type	Article

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