Received March 22, 2007
Revised April 23, 2007
Accepted after revision May 14, 2007

¹ School of Medicine of Ribeirao Preto - USP

^* To whom correspondence should be addressed. E-mail: antunes{at}fmrp.usp.br.

	Abstract

The presence of nitric oxide synthase (NOS), the enzyme that catalyses the formation of nitric oxide (NO), in the circumventricular organs and magnocellular neurons suggests an important role of NO in the modulation of vasopressin (AVP) and oxytocin (OT) release. Intracerebroventricular (icv) injection of angiotensin-II (ANG-II) stimulates the release of AVP, OT and atrial natriuretic peptide (ANP) and the associated antidiuretic and natriuretic effects. This study investigated the interaction between nitrergic and angiotensinergic pathways on the release of AVP, OT and ANP and urinary volume and sodium excretion in water-loaded rats. Male Wistar unanesthetized freely moving rats received two water loads followed by an injection into the lateral ventricle of an inhibitor of NOS (L-NAME), NO donors (SIN-1 or SNAP) or vehicle (isotonic saline) and, 20 min after, they received a second icv injection of ANG-II or vehicle. Injections of L-NAME or ANG-II produced an increase in AVP, OT and ANP plasma levels, and a reduction of urinary volume and an increase in sodium excretion. L-NAME pretreatment enhanced the ANG-II responses of increase in AVP, OT and ANP release, as well as the antidiuresis and natriuresis. Injection of SIN-1 or SNAP did not modify hormonal plasma levels and urinary parameters. In contrast, SNAP blocked the AVP, OT and ANP release, as well as antidiuretic and natriuretic responses induced by ANG-II. Thus, the central nitrergic system can act inhibiting the AVP, OT, ANP secretion and antidiuretic and natriuretic effects in response to ANG-II.

Key Words: Angiotensin, Nitric oxide, Vasopressin