Proceedings of The Physiological Society

University of Manchester (2010) Proc Physiol Soc 19, PC290

Poster Communications

Nitric oxide reduces hypo- and hyper- volemia-induced vasopressin and oxytocin mRNA expression in hypothalamic paraventricular and supra-optic nuclei.

W. L. Reis1, R. C. Rorato1, L. M. Bastianini1, L. L. Elias1, J. Antunes-Rodrigues1

1. Department of Physiology, School of Medicine of Ribeirao Preto - University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.

We have shown that central inhibition of nitric oxide syntase (NOS) increases plasma vasopressin (VP) and oxytocin (OT) concentrations, whereas nitric oxide (NO) donor reduces them in response to blood volume changes. We analyzed in hypothalamic paraventricular (PVN) and supra-optic (SON) nuclei the effects of acute hypo- and hypervolemic stimulation on mRNA expression of VP, OT and NOS, and the influence of NO donor or inhibitor in these expressions determined by Real Time PCR. Wistar male rats were anaesthetized with 2.5% tribromoethanol (1ml/100g, ip) for cannulas implant. The rats (5/group) were pretreated intracerebroventricular with vehicle (0.15M NaCl), NOS inhibitor (LNAME 250µg) or NO donor (SNAP 5µg), and 20min after, they were submitted to intra-arterial hypovolemia (hemorrhage, 15% of the total blood volume, 1ml/100g/min) or to intra-atrial extracellular blood volume expansion (BVE) with isotonic (0.15M NaCl) or hypertonic (0.30M NaCl) solution (2ml/100g/over 1min). Brains were collected by decapitation 60min after blood volume changes and the PVN and SON collected. The results are reported as mean±SEM and the data were analyzed by Two-Way analysis of variance followed by Newman-Keuls post-hoc test (differences at P<0.05). Values obtained from control rats were 1.0±0.2 arbitrary units (au). In the PVN and SON, hemorrhage induced an increase in VP (3.2±0.3au), OT (3.3±0.4au) and NOS (2.8±0.3au) mRNA expression. Pretreatment with LNAME did not change hemorrhage-induced VP and OT expressions, but it reduced NOS mRNA expression (1.1±0.2au). In contrast, SNAP decreased the VP (1.1±0.2au) and OT (1.2±0.2au) mRNA expression induced by hemorrhage, without effecting NOS expression in both structures. VP mRNA expression (3.4±0.4au) in both PVN and SON was increased by hypertonic BVE, but not isotonic BVE, and it was reduced by injection of SNAP (1.5±0.2au), while pretreatment with LNAME did not modify this expression. On the other hand, iso- and hypertonic BVE, induced an increase in OT (Iso 2.7±0.3au Hyper 2.5±0.3au) and NOS (Iso 2.2±0.2au Hyper 2.6±0.3au) mRNA expressions in the PVN and SON nuclei. Pretreatment with LNAME did not change iso- and hypertonic BVE-induced OT expression, but it reduced NOS mRNA expressions (Iso 0.9±0.1au Hyper 1.0±0.1au). On the contrary, SNAP decreased the OT mRNA expression (Iso 1.3±0.2au Hyper 1.1±0.2au) induced by BVE, without changing on NOS expression in both structures. Taking into account our previous results, the present data indicate that hypo- and hypervolemic stimulations increase VP, OT and NOS expression and, exogenous NO reduces VP and OT expression in response to hemorrhage or hypertonic BVE, suggesting an inhibitory modulation of NO in the control of neurohypophysial hormone synthesis and release during blood volume and plasma osmolality changes.

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