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- Title
Repeated administration of angiotensin II reduces its dipsogenic effect without affecting saline intake.
- Authors
Vento, Peter J.; Daniels, Derek
- Abstract
Angiotensin II (Ang II) acts at central type 1 (AT1) receptors to increase intake of water and saline. In vitro studies demonstrated rapid desensitization of the AT1 receptor after Ang II exposure, and behavioural studies in rats suggest that exposure to Ang II decreases the dipsogenic potency of subsequent Ang II. Nevertheless, the effect of repeated Ang II injections on saline intake remains untested, and a reliable protocol for examining this purported behavioural desensitization has not emerged from the literature. To address these issues, we established a reliable approach to study Ang II-induced dipsetic desensitization and used this approach to test the requirement of central AT1 receptors and the specificity of the effect for water intake. Rats given a treatment regimen of three injections of Ang II (300 ng, intracerebroventricular), each separated by 20 min, drank less water than control rats after a subsequent test injection of Ang II. The effect was relatively short lasting, dependent on the dose and timing of Ang II, and was almost completely blocked by the AT1 receptor antagonist losartan. In further testing, when rats were given access to both water and 1.5% saline, animals that received an Ang II treatment regimen drank less water than control animals, but saline intake was unaffected. These data support previous suggestions that Ang II-induced water and saline intakes are separable. Given the role of G protein uncoupling in desensitization of the AT1 receptor, these data are consistent with the emerging hypothesis that AT1 receptor G protein-dependent intracellular signalling pathways are more relevant for water, but not saline, intake.
- Subjects
ANGIOTENSINS; OLIGOPEPTIDES; SALINE solutions; HOMEOSTASIS; G proteins; RATS
- Publication
Experimental Physiology, 2010, Vol 95, Issue 6, p736
- ISSN
0958-0670
- Publication type
Article
- DOI
10.1113/expphysiol.2010.052191