Central angiotensin-(1-7) increases osmotic thirst.

Area of Science:

• Neuroendocrinology
• Physiology
• Molecular Biology

Background:

• Angiotensin-(1-7) [Ang-(1-7)], generated by ACE2, antagonizes the classical renin-angiotensin system but its role in hydromineral balance is unclear.
• Understanding Ang-(1-7)'s influence on thirst and water balance is crucial for comprehending neuroendocrine regulation.

Purpose of the Study:

• To investigate the effects of central Ang-(1-7) on basal and osmotically stimulated water intake in rats.
• To assess the role of Ang-(1-7) in neuroendocrine responses to hyperosmolality.

Main Methods:

• Rats were subjected to basal conditions, 24-hour water deprivation (WD), or 24-hour salt loading (SL).
• Intracerebroventricular (i.c.v.) injections of Ang-(1-7) or vehicle were administered.
• Water and salt intake, plasma vasopressin, and gene expression (Mas, Ace2) in brain regions (SFO, PVN, SON) were analyzed.

Main Results:

• Central Ang-(1-7) did not affect water or salt intake in control rats.
• Ang-(1-7) significantly increased water intake following WD and SL, without altering salt intake.
• WD increased Mas gene expression in the SON and PVN, while Ace2 mRNA levels remained unchanged.

Conclusions:

• Angiotensin-(1-7) enhances thirst perception and water intake specifically after osmotic stimuli, indicating a requirement for prior sensitization.
• The study identifies a novel function for Ang-(1-7) in osmotic thirst regulation, linked to increased Mas gene expression in the PVN and SON.
• These findings open avenues for further research into the mechanisms of Ang-(1-7) in hydromineral homeostasis.