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| Research article summary (published 29 Apr 1989): |
Hormonal response to blood volume expansion in diabetic subjects with and without autonomic neuropathy.
Full Abstract
The hormonal and renal response to volume expansion, produced by water immersion for 4 h, was studied in 14 insulin-dependent diabetic subjects (seven without complications, seven with autonomic neuropathy) and in 14 age-and-sex-matched normal control subjects. The diabetic subjects showed an impaired natriuretic response to volume expansion (total amount of sodium excreted 21 mmol compared to 39 mmol in normals, P less than 0.01) but the response did not differ in those with and without autonomic neuropathy. There was no significant difference in the suppression of plasma renin or aldosterone during immersion in either group. Plasma catecholamines suppressed on immersion in all groups. Basal values were lowest in the group with autonomic involvement. Atrial natriuretic peptide levels showed a twofold rise (from 4.8 to 9.6 pmol/l, P less than 0.01) on immersion. There was no significant difference in the levels of this hormone between diabetic patients and normal subjects or between those diabetics with and those without autonomic neuropathy. The present study confirms that diabetic subjects retain sodium avidly during volume expansion. This enhancement cannot be ascribed to any measurable difference in the levels of circulating hormones known to be involved in natriuresis and is not influenced by the presence of autonomic neuropathy.
Author information
Author/s: O'Hare, J P (JP); Anderson, J V (JV); Millar, N D (ND); Dalton, N (N); Tymms, D J (DJ); Bloom, S R (SR); Corrall, R J (RJ);
Affiliation: Department of Medicine, Bristol Royal Infirmary, London, UK.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Clinical endocrinology (Clin Endocrinol (Oxf)), published in ENGLAND. (Language: eng)
Reference: 1989-May; vol 30 (issue 5) : pp 571-9
Dates: Created 1990/02/09; Completed 1990/02/09; Revised 2006/11/15;
PMID: 2532573, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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