Premium
Central nitric oxide blocks vasopressin, oxytocin and atrial natriuretic peptide release and antidiuretic and natriuretic responses induced by central angiotensin II in conscious rats
Author(s) -
Reis Wagner Luis,
GiustiPaiva Alexandre,
Ventura Renato Rizo,
Margatho Lisandra Oliveira,
Gomes Dayane Aparecida,
Elias Lucila Leico Kagohara,
AntunesRodrigues José
Publication year - 2007
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2007.037911
Subject(s) - medicine , endocrinology , vasopressin , atrial natriuretic peptide , natriuresis , chemistry , oxytocin , antidiuretic , angiotensin ii , nitric oxide , renin–angiotensin system , nitric oxide synthase , excretion , receptor , blood pressure
The presence of nitric oxide synthase (NOS), the enzyme that catalyses the formation of nitric oxide (NO), in the circumventricular organs and magnocellular neurones suggests an important role of NO in the modulation of vasopressin (AVP) and oxytocin (OT) release. Intracerebroventricular ( i.c.v. ) injection of angiotensin II (Ang II) stimulates the release of AVP, OT and atrial natriuretic peptide (ANP), with the resultant antidiuretic and natriuretic effects. This study investigated the interaction between nitrergic and angiotensinergic pathways on the release of AVP, OT and ANP and on urinary volume and sodium excretion in water‐loaded rats. Unanaesthetized, freely moving, male Wistar rats received two water loads followed by an injection into the lateral ventricle of an inhibitor of NOS ( l ‐NAME), a NO donor [3‐morpholinylsydnoneimine chloride (SIN‐1) or S ‐nitroso‐ N ‐acetyl penicillamine (SNAP)] or vehicle (isotonic saline) and, 20 min after, they received a second i.c.v. injection of Ang II or vehicle. Injections of l ‐NAME or Ang II produced an increase in plasma levels of AVP, OT and ANP, a reduction in urinary volume and an increase in sodium excretion. Pretreatment with l ‐NAME enhanced the Ang II‐induced 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 to inhibit AVP, OT and ANP secretion and the antidiuretic and natriuretic effects in response to Ang II.