Effect of aprotinin on the renal response to vasopressin in diabetes insipidus rats.
The renal response to arginine vasopressin was investigated with and without the simultaneous administration of the kallikrein inhibitor, aprotinin, in conscious Brattleboro homozygous rats with hereditary diabetes insipidus. Arginine vasopressin caused a marked antidiuretic response (urinary osmolality increased from 118 to 739 mosmol/l) which was accompanied by a significant increase in urinary prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 182 and 441%, respectively). Kallikrein excretion remained unchanged after arginine vasopressin infusion. The infusion of aprotinin diminished urinary kallikrein activity to undetectable levels, decreased potassium excretion significantly and caused a slight fall in urinary prostaglandin excretion. However, aprotinin failed to modify the arginine vasopressin-induced enhancement in prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 168 and 442%, respectively), and the antidiuretic response was also similar to that observed under control conditions. These results indicate that the kallikrein-kinin system is not involved in the renal response to vasopressin in the Brattleboro rat.[1]References
- Effect of aprotinin on the renal response to vasopressin in diabetes insipidus rats. Fejes-Toth, G., Frölich, J.C., Naray-Fejes-Toth, A. J. Physiol. (Lond.) (1983) [Pubmed]
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