Dos-Santos Raoni Conceição, Monteiro Lívia da Rocha Natalino, Paes-Leme Bruno, Lustrino Danilo, Antunes-Rodrigues José, Mecawi André Souza, Reis Luís Carlos
Department of Physiological Sciences, Institute of Biological and Health Sciences, Federal Rural University of Rio de Janeiro, Seropédica, Rio de Janeiro, Brazil.
Department of Physiology, Federal University of Sergipe, Aracaju, Sergipe, Brazil.
Exp Physiol. 2017 Nov 1;102(11):1397-1404. doi: 10.1113/EP086417. Epub 2017 Oct 4.
What is the central question of this study? The central goal of this study was to understand the effects of central angiotensin-(1-7) on basal and osmotically stimulated water intake in rats. What is the main finding and its importance? This study demonstrated that central administration of angiotensin-(1-7) did not induce thirst in basal conditions but increased water intake after osmotic stimulation, such as water deprivation and salt loading. These results indicate a new function for this peptide, which, in turn, allows for future research on the mechanisms through which angiotensin-(1-7) influences osmotic thirst. Angiotensin-(1-7) [Ang-(1-7)] is generated by type 2 angiotensin-converting enzyme (ACE2) and binds to the MAS receptor. Although it is well known that Ang-(1-7) functionally antagonizes the effects of the classical renin-angiotensin system in several situations, the role of Ang-(1-7) in hydromineral homeostasis is not clear. The aim of this study was to assess the role of Ang-(1-7) on neuroendocrine responses to hyperosmolality in rats. Male Wistar rats were divided into the following three groups: control; 24 h of water deprivation (WD); and 24 h of salt loading (SL; 1.8% NaCl). Intracerebroventricular (i.c.v.) injections of Ang-(1-7) or vehicle were given to assess water intake and plasma concentration of vasopressin. Additionally, the brains from control and WD groups were collected to evaluate gene expression in the subfornical organ (SFO), paraventricular nucleus (PVN) and supraoptic nucleus (SON). It was found that i.c.v. Ang-(1-7) did not change water and salt intake in control rats; however, Ang-(1-7) increased water intake after WD and SL, with no change in salt intake. Plasma vasopressin was not changed by i.c.v. Ang-(1-7) in control or WD rats. Moreover, WD increased Mas gene expression in the SON and PVN, with no changes in Ace2 mRNA levels. In 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 the PVN and SON after water deprivation.
本研究的核心问题是什么？本研究的核心目标是了解中枢血管紧张素 -（1 - 7）对大鼠基础状态下以及渗透压刺激引起的饮水的影响。主要发现及其重要性是什么？本研究表明，中枢给予血管紧张素 -（1 - 7）在基础状态下不会诱发口渴，但在渗透压刺激后，如禁水和盐负荷增加时会增加饮水量。这些结果表明了该肽的一项新功能，这反过来又为未来研究血管紧张素 -（1 - 7）影响渗透压性口渴的机制提供了可能。血管紧张素 -（1 - 7）[Ang -（1 - 7）]由2型血管紧张素转换酶（ACE2）产生，并与MAS受体结合。尽管众所周知，在几种情况下Ang -（1 - 7）在功能上拮抗经典肾素 - 血管紧张素系统的作用，但其在水盐稳态中的作用尚不清楚。本研究的目的是评估Ang -（1 - 7）对大鼠高渗状态下神经内分泌反应的作用。雄性Wistar大鼠分为以下三组：对照组；禁水24小时（WD）；以及盐负荷24小时（SL；1.8% NaCl）。通过脑室内（i.c.v.）注射Ang -（1 - 7）或溶剂来评估饮水量和血管加压素的血浆浓度。此外，收集对照组和WD组的大脑，以评估穹窿下器官（SFO）、室旁核（PVN）和视上核（SON）中的基因表达。结果发现，脑室内注射Ang -（1 - 7）对对照组大鼠的水和盐摄入量没有影响；然而，Ang -（1 - 7）在禁水和盐负荷后增加了饮水量，而盐摄入量没有变化。脑室内注射Ang -（1 - 7）对对照组或禁水组大鼠的血浆血管加压素没有影响。此外，禁水增加了视上核和室旁核中Mas基因的表达，而Ace2 mRNA水平没有变化。总之，Ang -（1 - 7）在渗透压刺激后会增加口渴感，表明先前对其作用的致敏是必要的。这一发现与禁水后视上核和室旁核中Mas基因表达增加一致。
