Inhibition of sodium appetite by lipopolysaccharide: involvement of alpha(2)-adrenoceptors

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

FURO/CAP: A protocol for sodium intake sensitization

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride and sucrose intake in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Medial septal area ANG II receptor subtypes in the regulation of urine and sodium excretion induced by vasopressin

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Role of serotonergic 5-HT1A and oxytocinergic receptors of the lateral septal area in sodium intake regulation

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Vasopressin and angiotensin receptors of the medial septal area in the control of mean arterial pressure induced by vasopressin

Introduction. Brain arginine(8)-vasopressin (AVP), through the V-1a- and V-2-receptors, is essential for the maintenance of mean arterial pressure (MAP). Central AVP interacts with the components of the renin-angiotensin system, which participate in MAP regulation. This study all to determine the effects of V-1a-, V-2- and V-1a/V-2-AVP selective antagonists and AT(1)- and AT(2)-angiotensin II (Ang II) selective antagonists on the MAP induced by AVP injected into the medial septal area (MSA) of the brain.Materials and methods. Male Holtzman rats with stainless steel cannulae implanted into the MSA were used in experiments. Direct MAP was recorded in Conscious rats.Results. AVP administration into the MSA caused a prompt and potent pressor response in a dose-dependent fashion. Pretreatment with the V-1a- and V-2-antagonists reduced, whereas prior injection of the V-1a/V-2-antagonist induced a decrease in the MAP that remained below the baseline. Both AT(1)- and AT(2)-antagonists elicited a decrease, While simultaneous injections of two antagonists were more effective in decreasing the MAP induced AVP.Conclusion. These results indicate there is a synergism bell the V-1a- and V-2-AVP, and AT(1)- AT, and AT(2)-Ang II receptors in the MSA in the regulation of MAP.

Activation of alpha(2)-adrenoceptors in the lateral hypothalamus reduces pilocarpine-induced salivation in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Switching control of sympathetic activity from forebrain to hindbrain in chronic dehydration

We investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t) SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e. g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed up-regulation of AP1 transcription factor JunD in the dehydrated cNTS, we tested the hypothesis that AP1 transcription factor activity is responsible for dehydration-induced functional plasticity. When AP1 activity was blocked in the cNTS using a viral vector expressing a dominant negative FosB, cNTS inactivation was ineffective. However, tSNA was decreased after pre-collicular transection, a response similar to that seen in EHrats. Thus, the dehydration-induced switch in control of tSNA from hypothalamus to cNTS seems to be mediated via activation of AP1 transcription factors in the cNTS. If AP1 activity is blocked in the cNTS during dehydration, sympathetic activity control reverts back to forebrain regions. This unique reciprocating neural structure-switching plasticity between brain centres emphasizes the multiple mechanisms available for the adaptive response to dehydration.