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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
VASOTOCIN ANALOGUES WITH SELECTIVE EFFECT ON RENAL NA+, K+ OR WATER EXCRETION
Abstract number: P31
KUTINA1 AV, MARINA1 AS
1Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, 194223 Saint-Petersburg, 44 Pr. Thoreza, Russia
Vasopressin and nonmammalian hormone vasotocin are known to increase water permeability of mammalian collecting ducts, frog skin and urinary bladder. Neurohypophyseal nonapeptides have also shown to interfere in the regulation of renal ion transport. The subject of these studies was a search for peptides selectively regulating renal water, Na+ and K+ excretion. We tested vasotocin analogues modified at positions 1, 4 and 8: 1- deamino-vasotocin (dAVT), 1-deamino-4-Arg- vasotocin (dAAVT), 1-deamino-8-DArg-vasotocin, 1- deamino-4-Arg-8-DArg-vasotocin. Effects on water, Na+ and K+ transport were evaluated in experiments with normal and water loaded Wistar rats. It was shown that the dAVT possessed evident antidiuretic, natriuretic and kaliuretic activities. Substitutions in the 4th and 8th positions increased the selectivity of peptides action. The Arg4 and DArg8 analogues were antidiuretic but not natriuretic. The Arg4 peptides induced kaliuresis without any effect on Na+ excretion. A selective V1a-agonist reproduced the renal effects of dAVT on Na+ and K+ excretion, whereas a V1a- antagonist significantly reduced the dAVT- stimulated natriuresis and did not influence on the dAVT- and dAAVT-induced kaliuresis. It is assumed that action of the nonapeptides on Na+ and K+ transport is independent of their V2 antidiuretic activity and mediated by different types of V-receptors (the V1a receptor for natriuretic effect and unknown one for kaliuretic). In accordance to the data obtained, neurohypophyseal hormones might take part in the selective regulation of Na+ and K+ excretion. The work was supported by the RFBR (¹ 11-04- 01636a) and the Program of the Department of physiology and fundamental medicine of RAS.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :P31