Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat

in Journal of Endocrinology
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J. A. Charlton
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C. J. Thompson
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P. H. Baylis
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ABSTRACT

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA.

Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3–4 units protamine–zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11·4 pmol/l compared with 1·6 pmol/l; P <0·05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, β-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P <0·05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = +0·75; P <0·01), and plasma ketone bodies and plasma AVP (r= +0·60; P <0·05) were obtained. The increase in plasma AVP in the DKA group was not due to haemodynamic changes or nausea/emesis. The results suggest that in early DKA in the rat, increases in the plasma concentration of AVP are related to the metabolic consequences of insulin deficiency and not to hypovolaemia or hypotension.

J. Endocr. (1988) 116, 343–348

 

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