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Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes

Lookup NU author(s): Professor Peter Baylis


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Renal resistance to vasopressin has been demonstrated in type 1 diabetes and in type 2 diabetes with nephropathy. However, renal response to vasopressin in type 2 diabetes without nephropathy has not been studied. We studied 10 subjects with poorly controlled type 2 diabetes (PCDS; Hb A(1c) > 9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A(1c) <7%), and 10 matched nondiabetic control subjects (NDCS) during a euglycemic 8-h water deprivation test. None of the subjects had nephropathy. Water deprivation caused similar rises in plasma vasopressin concentrations in all three groups, but the rise in urine osmolality in PCDS (280.3 &PLUSMN; 49.7 to 594.4 &PLUSMN; 88.5 mosmol/kgH(2)O) was lower than in WCDS (360.7 &PLUSMN; 142.8 to 794.1 &PLUSMN; 77.3 mosmol/kgH(2)O, P <0.001) or NDCS (336.0 +/- 123.3 to 786.5 +/- 63.3 mosmol/kgH(2)O, P = 0.019). Total urine output was higher in the PCDS than in WCDS and NDCS (P < 0.05). Linear regression analysis showed that, in PCDS, the osmotic thresholds for thirst (291.9 &PLUSMN; 4.6 mosmol/kgH(2)O) and vasopressin release (291.1 &PLUSMN; 2.9 mosmol/kgH(2)O) were higher compared with WCDS (286.6 &PLUSMN; 1.8 and 286.0 &PLUSMN; 3.6 mosmol/kgH(2)O, respectively) and NDCS (286.0 &PLUSMN; 2.4 and 284.1 &PLUSMN; 4.7 mosmol/kgH(2)O, respectively) (between groups P < 0.001 for both variables). Under conditions of euglycemia, PCDS have impaired renal response to vasopressin and elevated osmotic threshold for thirst and vasopressin release in response to dehydration. Under conditions of chronic hyperglycemia, these abnormalities may significantly contribute to the development of dehydration in PCDS.

Publication metadata

Author(s): Agha A, Smith D, Finucane F, Sherlock M, Morris A, Baylis P, Thompson CJ

Publication type: Article

Publication status: Published

Journal: American Journal of Physiology: Endocrinology and Metabolism

Year: 2004

Volume: 287

Issue: 6

Pages: E1100-E1106

ISSN (print): 0193-1849

ISSN (electronic): 1522-1555

Publisher: American Physiological Society


DOI: 10.1152/ajpendo.00214.2004


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