Rats were administered streptozocin (STZ; 50 or 75 mg/kg i.v., tail vein) or vehicle. Approximately 2 wk later, venous and arterial catheters were implanted for subsequent (24 h later) vasopressin, electrolyte, and hemodynamic measurements. STZ-induced diabetic (STZ-D) rats demonstrated a dose-dependent increase in the plasma glucose concentration, plasma osmolality, and plasma vasopressin concentration. Mean arterial blood pressure (MABP) was unchanged, but heart rate was reduced. Diabetes-prone BB rats, maintained on or withdrawn from insulin treatment for 24–48 h, and diabetes-resistant rats were instrumented and studied as above. Spontaneous-diabetes–prone rats demonstrated increases in plasma glucose concentration and plasma osmolality similar to STZ-D rats but had significantly greater plasma vasopressin concentrations. The significant decrease in MABP observed in these animals probably contributed to the enhanced vasopressin response. We conclude that both osmotic and cardiovascular parameters play important roles in vasopressin secretion in diabetic rats.
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Original Articles|
January 01 1989
Vasopressin in Rats With Genetic and Streptozocin-Induced Diabetes
David P Brooks;
David P Brooks
Department of Physiology and Biophysics, University of Tennessee
Memphis, Tennessee
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David F Nutting;
David F Nutting
Department of Physiology and Biophysics, University of Tennessee
Memphis, Tennessee
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Joan T Crofton;
Joan T Crofton
Department of Physiology and Biophysics, University of Tennessee
Memphis, Tennessee
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Leonard Share
Leonard Share
Department of Physiology and Biophysics, University of Tennessee
Memphis, Tennessee
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Address correspondence and reprint requests to Dr. David P. Brooks, Department of Pharmacology, L521, Smith Kline & French Laboratories, P.O. Box 1539, King of Prussia, PA 19406–0939.
Diabetes 1989;38(1):54–57
Article history
Received:
November 13 1987
Revision Received:
July 12 1988
Accepted:
July 12 1988
PubMed:
2909412
Citation
David P Brooks, David F Nutting, Joan T Crofton, Leonard Share; Vasopressin in Rats With Genetic and Streptozocin-Induced Diabetes. Diabetes 1 January 1989; 38 (1): 54–57. https://doi.org/10.2337/diab.38.1.54
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