TY - JOUR
T1 - Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes
AU - Agha, Amar
AU - Smith, Diarmuid
AU - Finucane, Francis
AU - Sherlock, Mark
AU - Morris, Andrew
AU - Baylis, Peter
AU - Thompson, Christopher J.
PY - 2004/12/1
Y1 - 2004/12/1
N2 - 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 A1c >9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A ic <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 ± 49.7 to 594.4 ± 88.5 mosmol/kgH2O) was lower than in WCDS (360.7 ± 142.8 to 794.1 ± 77.3 mosmol/kgH2O, P < 0.001) or NDCS (336.0 ± 123.3 to 786.5 ± 63.3 mosmol/kgH2O, 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 ± 4.6 mosmol/kgH2O) and vasopressin release (291.1 ± 2.9 mosmol/kgH2O) were higher compared with WCDS (286.6 ± 1.8 and 286.0 ± 3.6 mosmol/kgH2O, respectively) and NDCS (286.0 ± 2.4 and 284.1 ± 4.7 mosmol/kgH2O, 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.
AB - 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 A1c >9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A ic <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 ± 49.7 to 594.4 ± 88.5 mosmol/kgH2O) was lower than in WCDS (360.7 ± 142.8 to 794.1 ± 77.3 mosmol/kgH2O, P < 0.001) or NDCS (336.0 ± 123.3 to 786.5 ± 63.3 mosmol/kgH2O, 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 ± 4.6 mosmol/kgH2O) and vasopressin release (291.1 ± 2.9 mosmol/kgH2O) were higher compared with WCDS (286.6 ± 1.8 and 286.0 ± 3.6 mosmol/kgH2O, respectively) and NDCS (286.0 ± 2.4 and 284.1 ± 4.7 mosmol/kgH2O, 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.
KW - osmoregulation
UR - http://www.scopus.com/inward/record.url?scp=8544268673&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.00214.2004
DO - 10.1152/ajpendo.00214.2004
M3 - Article
C2 - 15292031
AN - SCOPUS:8544268673
SN - 0193-1849
VL - 287
JO - American Journal of Physiology-Endocrinology and Metabolism
JF - American Journal of Physiology-Endocrinology and Metabolism
IS - 6 50-6
ER -