The hydroelectrolytic homeostasis is constantly regulated by informations concerning the body fluids volume and the concentration of ions. Changes in osmolality are detected by receptors located in several regions of the central nervous system (CNS), including the circumventricular organs. Conformational changes in these cells activate neurons located in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus, which secretion includes oxytocin (OT) and vasopressin (AVP). The raise in plasma osmolality causes a proportional increase in the plasma OT concentration, which induces the excretion of sodium and chloride and stimulates the ANP secretion by cardiomyocites. These hormones are involved in the salt intake, being released into the circulation in response to osmotic stimuli. Several neurotransmitters are involved in the control of AVP and OT release, such as nitric oxide (NO). NO is an important signaling molecule which seems to modulate several physiological processes as neurotransmission, vasodilation and behavioral responses, and has been suggested to exert a prominent regulatory role on hypothalamic-pituitary system. NO acts as an important signaling molecule and effector of various physiological processes such as neurotransmission, vasodilation and behavioral responses. However, there are conflicting data on the role of NO in the release of AVP and OT and studies are scarce and controversial. Thus, knowing the importance of nitric oxide signaling in the regulation of neuroendocrine responses, the results to be obtained will elucidate the physiological relevance of NO of neuronal origin on neuroendocrine responses in the paradigm of salt loaded in male rats in adulthood. Appetitive behavior and excretion of water and electrolytes will be assessed as well as the secretion of neurohypophyseal hormones, vasopressin, oxytocin, angiotensin II, corticosterone and prolactin in basal conditions and in response to osmotic stimulus salt loaded and physical restraint stress after use of a drug selective nNOS inhibitor or the inhibition of nNOS enzyme obtained from a viral vector .
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