Central angiotensin 1–7 increases osmotic thirst

Abstract

Introduction

Angiotensin 1–7 (ANG 1–7) is generated by type 2 angiotensin converting enzyme (ACE 2) and binds to MAS receptor. Although it is well known that angiotensin 1–7 functionally antagonizes the effects of the classical renin-angiotensin system (RAS) in several situations, the role of ANG 1–7 in hydromineral homeostasis is not clear. This study aimed to assess the role of ANG 1–7 on neuroendocrine responses to hyperosmolality in rats.

Methods

Male Wistar rats were divided into the following three groups: control, 24 hours of water deprivation (WD) and 24 hours of salt loading (SL, 1.8% NaCl). Intracerebroventricular (icv) injections of ANG 1–7 or vehicle were given to assess water intake and vasopressin (AVP) plasma levels. Additionally, the brains from control and WD groups were collected to evaluate gene expression in the subfornical (SFO), paraventricular (PVN), and supraoptic (SON) nuclei.

Results

Icv ANG 1–7 did not change water and salt intake in control rats; however, ANG 1–7 increased water intake following WD and SL, with no change in salt intake. Plasma AVP was not changed by icv ANG 1–7 in control or WD rats. Moreover, WD increased MAS gene expression in the SON and PVN, with no changes in ACE 2 mRNA levels.

Conclusion

ANG 1–7 increases thirst after osmotic stimuli, indicating that a previous sensitization to its action is necessary. This finding is consistent with the increased MAS gene expression in PVN and SON after water deprivation.

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