Effect of injection of ANG II into the lateral parabrachial nucleus (LPBN) on hypertonic NaCl and water intake

• Grant number: 10/17822-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: February 01, 2011
• End date: December 31, 2011
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: João Carlos Callera
• Grantee: Gabriela Patrício Bearare
• Host Institution: Faculdade de Odontologia (FOA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil

Abstract

The lateral parabrachial nucleus (LPBN), a structure in the rat that lies dorsolateral to the superior cerebellar peduncle, is an important inhibitory area involved in the control of water and sodium intake. A potent substance that cause thirst and sodium appetite is a neuropeptide angiotensin II (ANG II), when production is made by hypovolemia and hypotension. The main action of ANG II is the subfornical organ, AV3V, area postrema, parabrachial nucleus (PBN) and nucleus of the solitary tract (NTS). The receptors for ANG II are the AT1 and AT2. Electrolytic lesions of the LPBN display increased water intake in response to central and peripheral injection of ANG II, the blockade of serotonin and cholecystokinin receptors of the LPBN increased water and sodium intake, suggested that exist an area that control inhibition of sodium appetite. Previous studies evaluated the effects of GABA receptors of LPBN on water and sodium intake in satiated and depleted-sodium rats. These studies showed that GABA receptors activation induced water and NaCl intake, responses that was reduced by previous injections of angiotensin antagonist losartan(the AT1 receptor antagonist). Considering no evidence in the literature showing the effects of ANG II into the LPBN on water and sodium intake, the main aim of the present study is evaluate the injection of ANG II into the bilateral LPBN on water and sodium intake in satiated and sodium-depleted rats (extracellular dehydration model)