Influence of nitric oxide synthase inhibition on vasopressin and corticosterone secretion during water deprivation in rats

Abstract

Nitric oxide (NO) is a short-lived radical that functions as a neurotransmitter in the central nervous system and plays a physiological role in the regulation of hypothalamic-pituitary-adrenal axis and vasopressinergic axis. In the present study, we aimed to investigate the interaction between the generation of NO and vasopressin (AVP) and corticosterone release after 3 days of water deprivation in rats. Animals were previously treated with intraperitoneal (i.p.) saline or L-nitro-arginine methyl ester (L-NAME) injection. L-NAME is a nonspecific inhibitor of nitric oxide synthases. In control rats given i.p. saline or L-NAME, hypothalamic, pituitary, and plasma AVP levels and plasma corticosterone did not change from baseline levels (p>0.05). Three days of water deprivation increased significantly the corticosterone levels in plasma (p<0.01) and AVP levels in hypothalamus and plasma (p<0.01), but not in pituitary, which showed a significant decrease. These variations were concomitant with the elevation of nitrates/nitrates in plasma. L-NAME injection abolished significantly (p<0.01) the elevation of plasma corticosterone and hypothalamic AVP levels induced by water deprivation. These findings showed that in water-deprived rats, nitric oxide synthase inhibition by L-NAME inhibits corticosterone and vasopressin release, suggesting a potent stimulatory role of NO.

Reconsolidation may incorporate state-dependency into previously consolidated memories

“…Water deprivation influences a whole plethora of physiological functions such as increase of corticoid secretion (Mornagui et al 2010) and arginine-vasopressin levels (Knight et al 2010), osmolality dysregulation (Stricker et al 2002), increase of plasma renin activity (Nagai et al 1993) and sodium concentration (De Luca et al 2010), decrease of urinary volume (Jorgensen et al 1993), and alterations in brain expression of angiotensinconverting enzyme (Bourassa and Speth 2010). However, we show that the induction of state-dependent memories may be supported, e.g., by the renin -angiotensin system (RAS), since the water deprivation effects were replicated by the infusion of ANGII into the hippocampus.…”

The Role of Nitric Oxide in the Dysregulation of the Urine Concentration Mechanism in Diabetes Mellitus

“…In our study, DM animals treated with l -NAME had no compensatory increase in AQP2 expression. Nitric oxide synthase inhibition by l -NAME has been shown to inhibit vasopressin release (Mornagui et al, 2010), perhaps explaining the lowered levels of AQP2 expression the treated DM animals.…”