Interaction between supraoptic nucleus and septal area in the control of water, sodium intake and arterial blood pressure induced by injection of angiotensin II

Saad, Wilson Abrão; Camargo, Laa; Guarda, Ismael Francisco Motta Siqueira; Santos, Talmir Augusto Faria Brizola dos; Guarda, Renata Saad; Saad, William Abrão; Simões, Silvio Jorge Coelho; Rodrigues, Josemar

doi:10.1016/j.pbb.2004.01.013

Cited by 17 publications

(10 citation statements)

References 27 publications

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“…The circumventricular organs, including the SFO and organum vasculosum of the laminae terminalis (OVLT) and median preoptic nucleus (MnPO) play an important role in the control of thirst and sodium appetite [33]. In fact, SFO is the main target for ANG-II to stimulate water and salt intake, and it is also involved in the control of blood pressure and neurohypophysial secretion [3,4]. It has been postulated that ANG-II-induced water and sodium intake can be explained, at least in part, by the increase in VP content and neurotransmitter release from axons of neurons onto the effector neurons of drinking responses [34].…”

Section: Discussionmentioning

confidence: 99%

“…It has been postulated that ANG-II-induced water and sodium intake can be explained, at least in part, by the increase in VP content and neurotransmitter release from axons of neurons onto the effector neurons of drinking responses [34]. Treatment with V1 receptor antagonist was shown to cause a marked decrease in water ingestion, but not sodium appetite, induced by angiotensinergic activation [4]. …”

Section: Discussionmentioning

confidence: 99%

“…The drugs were injected in 0.5 μl volumes over a time period of 30-60 seconds. All doses used in this study were based on previous reports in the literature [4,26]. …”

Section: Methodsmentioning

confidence: 99%

“…In fact, the expression of NOS gene was increased in the same structures related with ANG-II actions after hypovolemia [14,15] and dehydration [16-18]. Furthermore, the inhibition of endogenous NOS enhances drinking behavior and cardiovascular responses induced by the central administration of ANG II [4,19]. On the other hand, L-arginine, a precursor of NO, as well as NO donors, were able to reduce VP and OT release, water intake, blood pressure, diuretic and natriuretic effects of central angiotensinergic stimulation [4,20-22].…”

Section: Introductionmentioning

confidence: 99%

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Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

Reis

Saad

Camargo

et al. 2010

Behavioral and Brain Functions

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BackgroundNitric oxide (NO) synthesis has been described in several circumventricular and hypothalamic structures in the central nervous system that are implicated in mediating central angiotensin-II (ANG-II) actions during water deprivation and hypovolemia. Neuroendocrine and cardiovascular responses, drinking behavior, and urinary excretions were examined following central angiotensinergic stimulation in awake freely-moving rats pretreated with intracerebroventricular injections of Nω-nitro-L-arginine methyl ester (L-NAME, 40 μg), an inhibitor of NO synthase, and L-arginine (20 ug), a precursor of NO.ResultsInjections of L-NAME or ANG-II produced an increase in plasma vasopressin (VP), oxytocin (OT) and atrial natriuretic peptide (ANP) levels, an increase in water and sodium intake, mean arterial blood pressure and sodium excretion, and a reduction of urinary volume. L-NAME pretreatment enhanced the ANG-II response, while L-arginine attenuated VP and OT release, thirst, appetite for sodium, antidiuresis, and natriuresis, as well as pressor responses induced by ANG-II.Discussion and conclusionThus, the central nitrergic system participates in the angiotensinergic responses evoked by water deprivation and hypovolemia to refrain neurohypophysial secretion, hydromineral balance, and blood pressure homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The drugs were injected in 0.5 μl volumes over a time period of 30-60 seconds. All doses used in this study were based on previous reports in the literature [4,26]. …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

Reis

Saad

Camargo

et al. 2010

Behavioral and Brain Functions

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“…As mentioned in the Introduction (11), the septal‐preoptic region has been implicated in ingestive behaviours induced by local application of Ang II (38) and other dipsogenic stimuli (39) in different strains of rat; thus, to find neurones responsive to Ang II in the present study should be considered normal. However, these same injections have not been made in behaving Fischer rats to investigate whether these rats are as responsive as the other strains.…”

Section: Discussionmentioning

confidence: 92%

Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Omouessi

Falconetti

Chapleur

et al. 2006

J Neuroendocrinology

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Central administration of angiotensin (Ang) II stimulates thirst and sodium intake via the AT-1 receptor. Mineralocorticoid pretreatment enhances Ang II-induced drinking of hypertonic salt solutions (i.e. the synergy theory) in Wistar and Sprague-Dawley rats. Electrophysiological experiments using iontophoretic application of Ang II, and the AT-1 receptor specific nonpeptide antagonist losartan, have shown excitation of neurones in the preoptic/medial septum region of urethane anaesthetised male Wistar rats. Deoxycorticosterone acetate (DOCA) pretreatment further enhanced this neuronal excitation to Ang II and reduced the responses to losartan. This generated the hypothesis that DOCA-enhanced Ang II-induced neuronal excitation was necessary for the enhanced salt intake of synergy theory. We tested this hypothesis in Fischer 344 rats that are known to have a low basal salt appetite and reduced sensitivity for i.c.v. Ang II. We compared the effect of DOCA pretreatment on i.c.v. Ang II-induced water and 2% NaCl intake in behaving adult male, Fischer rats, as well as preoptic/medial septum region neuronal responses to Ang II and losartan, using a seven-barrelled micro-iontophoretic electrode sealed to a recording electrode in urethane anaesthetised, male Fischer rats. Two groups were used: one pretreated with DOCA (0.5 mg/day for 3 days) and the other comprising controls, treated with isotonic saline. Ang II applied iontophoretically increased activity in 31% of the spontaneously active neurones. Following DOCA pretreatment, the responsiveness to Ang II (when applied after aldosterone) was increased. By contrast, in the behaving animals, water and 2% NaCl intake in response to i.c.v. Ang II were not enhanced by DOCA pretreatment. These results do not support the working hypothesis but could be interpreted as evidence for the existence of two separately modulated central Ang II systems: one responding to mineralocorticoids with increased neuronal activity and the other responsible for the Ang II-induced sodium appetite in conscious rats.

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Neuroendocrine Regulation of Hydromineral Homeostasis

Mecawi

Ruginsk

Elias

et al. 2015

Comprehensive Physiology

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Since the crucial evolutionary change from an aqueous to a terrestrial environment, all living organisms address the primordial task of equilibrating the ingestion/production of water and electrolytes (primarily sodium) with their excretion. In mammals, the final route for the excretion of these elements is mainly through the kidneys, which can eliminate concentrated or diluted urine according to the requirements. Despite their primary role in homeostasis, the kidneys are not able to recover water and solutes lost through other systems. Therefore, the selective stimulation or inhibition of motivational and locomotor behavior becomes essential to initiate the search and acquisition of water and/or sodium from the environment. Indeed, imbalances affecting the osmolality and volume of body fluids are dramatic challenges to the maintenance of hydromineral homeostasis. In addition to behavioral changes, which are integrated in the central nervous system, most of the systemic responses recruited to restore hydroelectrolytic balance are accomplished by coordinated actions of the cardiovascular, autonomic and endocrine systems, which determine the appropriate renal responses. The activation of sequential and redundant mechanisms (involving local and systemic factors) produces accurate and self-limited effector responses. From a physiological point of view, understanding the mechanisms underlying water and sodium balance is intriguing and of great interest for the biomedical sciences. Therefore, the present review will address the biophysical, evolutionary and historical perspectives concerning the integrative neuroendocrine control of hydromineral balance, focusing on the major neural and endocrine systems implicated in the control of water and sodium balance.

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Interaction between supraoptic nucleus and septal area in the control of water, sodium intake and arterial blood pressure induced by injection of angiotensin II

Cited by 17 publications

References 27 publications

Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Neuroendocrine Regulation of Hydromineral Homeostasis

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