Drinking in juvenile Atlantic salmon (Salmo salar L.) in response to feeding and activation of the endogenous renin-angiotensin system

Drinking rate and rectal fluid production of juvenile Atlantic salmon (1-2 g) in freshwater were investigated in unfed fish and recently fed fish. Drinking was also investigated following activation of the renin-angiotensin system (RAS) by two hypotensive agents, a nitric oxide (NO) donor sodium nit...

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Bibliographic Details
Published in:Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology
Main Author: Eddy, F. Brian
Format: Article in Journal/Newspaper
Language:English
Published: 2007
Subjects:
Online Access:https://discovery.dundee.ac.uk/en/publications/e2c1d506-2b5d-41aa-aac9-7c975f1f1c1f
https://doi.org/10.1016/j.cbpa.2006.08.004
http://www.elsevier.com/locate/cbpa
Description
Summary:Drinking rate and rectal fluid production of juvenile Atlantic salmon (1-2 g) in freshwater were investigated in unfed fish and recently fed fish. Drinking was also investigated following activation of the renin-angiotensin system (RAS) by two hypotensive agents, a nitric oxide (NO) donor sodium nitroprusside (SNP) and bacterial lipopolysaccharide (LPS). In unfed fish the basal drinking rate was 0.13 µL g -1 h -1 and rectal fluid production was 0.076 µL g -1 h -1 . In recently fed fish both drinking rate and rectal fluid production increased significantly by about fivefold compared to unfed fish, and similar values were obtained for fish exposed to PS for 24 h. Exposure to SNP resulted in about a tenfold elevation of drinking rate and rectal fluid production, compared to unfed fish. Absorption of water by the gut was in the range 35-60% for all treatments. Drinking may have a role in processing food in the gut and the fluid in the gut may subjected to absorptive and secretory processes. The most likely route for removal of water absorbed by the gut is excretion via the kidney and this would result in an increased osmoregulatory burden on the fish. In polluted waters drinking could be increased through stimulation of the endogenous RAS by vasodilators, e.g., LPS and the gut could be a significant target for toxin exposure.