Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II.

W.A Saad,T.A.F.B Santos,L.A.A Camargo,I.F.M.S Guarda,Willian A Saad,S Simões

doi:10.1590/s0100-879x2002000800012

Abstract

We investigated the role of alpha-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na+, K+ and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/ micro l) increased water intake (12.5 +/- 1.7 ml/120 min). Clonidine (20 nmol/ micro l) injected into the MSA reduced the ANGII-induced water intake (2.9 +/- 0.5 ml/120 min). Pretreatment with 80 nmol/ micro l yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 +/- 0.4 and 3.1 +/- 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGII-induced water intake (0.2 +/- 0.1 and 0.2 +/- 0.1 ml/120 min, respectively). ANGII reduced Na+ (23 +/- 7 micro Eq/120 min), K+ (27 +/- 3 micro Eq/120 min) and urine volume (4.3 +/- 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of alpha1- and alpha2-antagonists decreased ANGII-induced water intake, and abolished the Na+, K+ and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal alpha1- and alpha2-adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII.

Highlights

Central administration of angiotensin II (ANGII) induces thirst in satiated animals by interacting with neurotransmitters, especially catecholamines [1,2]
The present results show that the α2adrenoceptor agonist clonidine injected into the medial septal area (MSA) attenuated the dipsogenic response produced by ANGII injection into the 3rdV
The inhibitory and facilitatory effects of noradrenaline injected into the central nervous system on ingestive behavior suggest a dual role for noradrenaline in the central control of water and salt intake induced by ANGII [27]

Summary

Introduction

Central administration of angiotensin II (ANGII) induces thirst in satiated animals by interacting with neurotransmitters, especially catecholamines [1,2]. Adrenergic neurotransmitters from several hypothalamic areas may participate in the effect of ANGII regulating hydromineral fluid intake and renal electrolyte excretion in a process that involves α1and α2-adrenoceptors [3,4,5]. Previous studies have demonstrated the effects of α-antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by ANGII injection into the subfornical organ [3]. In view of the importance of the circumventricular structures and MSA for the hydromineral balance in rats [9,25], as well as the important interactions between areas of the circumventricular structures and the MSA, we determined the effect of the injection of clonidine, yohimbine and prazosin into the MSA on water intake and on the antinatriuretic, antikaliuretic and antidiuretic effects induced by the administration of ANGII into the third ventricle (3rdV)

Material and Methods

Results

Discussion