Roles of brain angiotensins II and III in thirst and sodium 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 pr...
Saved in:
Published in | Brain research Vol. 1060; no. 1; pp. 108 - 117 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Elsevier B.V
26.10.2005
Amsterdam Elsevier New York, NY |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | 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. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-8993 1872-6240 0006-8993 |
DOI: | 10.1016/j.brainres.2005.08.032 |