Roles of brain angiotensins II and III in thirst and sodium appetite

Wendy L Wilson; Bernard P Roques; Catherine Llorens-Cortes; Robert C Speth; Joseph W Harding; John W Wright

doi:10.1016/j.brainres.2005.08.032

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Roles of brain angiotensins II and III in thirst and sodium appetite

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Roles of brain angiotensins II and III in thirst and sodium appetite

Wendy L Wilson, Bernard P Roques, Catherine Llorens-Cortes, Robert C Speth, Joseph W Harding and John W Wright

Brain research, Vol.1060(1), pp.108-117

2005

DOI: https://doi.org/10.1016/j.brainres.2005.08.032

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https://hdl.handle.net/2376/107469

PMID: 16182260

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Abstract

Thirst

Captopril

AngIII

Furosemide

Angiotensin

Salt appetite

The current study examined the effects of intracerebroventricular (icv) infused aminopeptidase-resistant analogs of angiotensin II (AngII) and angiotensin III (AngIII) on thirst and sodium appetite. The analogs, [D-Asp 1D-Arg 2]AngII and [D-Arg 1]AngIII, were further protected from degradation by pretreatment with the aminopeptidase A inhibitor, EC33, or the aminopeptidase N inhibitor, PC18. Prior to icv infusions, rats were sodium depleted with furosemide, followed by the angiotensin-converting enzyme inhibitor captopril, to block endogenous angiotensin formation. Both angiotensin analogs, at either of the two doses, were capable of eliciting fluid intakes of water and 0.3 M NaCl. Water and saline intakes were increased to a similar extent by 125 and 1250 pmol of [D-Asp 1D-Arg 2]AngII. [D-Arg 1]AngIII produced a dose-dependent increase in water intake, whereas saline intake was equivalently increased by the 125 and 1250 pmol infusions. Pretreatment with EC33 or PC18 decreased water and saline intakes in response to [D-Asp 1D-Arg 2]AngII, while pretreatment with PC18 altered the time course of the [D-Arg 1]AngIII-induced water and saline intakes. The ability of both inhibitors to decrease, but not completely block, AngII analog-induced intakes, coupled with the altered time course of the responses induced by the AngIII analog in the presence of PC18, supports the hypothesis that both AngII and AngIII are active ligands in brain angiotensin-mediated thirst and sodium appetite. However, these results do not resolve the primary question of whether conversion of AngII to AngIII is a prerequisite to dipsogenic and salt appetite responses in the brain.

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Title: Roles of brain angiotensins II and III in thirst and sodium appetite
Creators: Wendy L Wilson - Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA
Bernard P Roques - Department de Pharmacochimie Moleculaire et Structurale, Institut National de la Santé et de la Recherche Médicale, Unite 266, Centre National de la Recherche Scientifique, UMR 8600, 75270 Cedex 06, Paris
Catherine Llorens-Cortes - Institut National de la Santé et de la Recherche Médicale, Unit 691, College de France, 75231 Cedex 05, Paris
Robert C Speth - Department of Pharmacology, and Research Institute in Pharmaceutical Sciences, University of Mississippi, University, MS 38677, USA
Joseph W Harding - Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA
John W Wright - Department of Psychology, Washington State University, Pullman, WA 99164-4820, USA
Publication Details: Brain research, Vol.1060(1), pp.108-117
Academic Unit: Psychology, Department of; Integrative Physiology and Neuroscience, Department of
Publisher: Elsevier B.V
Identifiers: 99900547388101842
Language: English
Resource Type: Journal article