PERSONAL DE APOYO
ELESGARAY Rosana
congresos y reuniones científicas
Título:
NITRIC OXIDE AS A KEY MEDIATOR OF VASCULAR ACTIONS OF ATRIAL NATRIURETIC PEPTIDE IN SPONTANEOUSLY HYPERTENSIVE RATS.
Autor/es:
CANIFFI CAROLINA; ELESGARAY ROSANA; RODRÍGUEZ IERACE DANIELA; SAVIGNANO L; AGUIRRE SOFÍA; ARRANZ CRISTINA; COSTA MARÍA ÁNGELES
Reunión:
Congreso; XVII Meeting ISHR Latin American Section. International Society for Heart Research.; 2009
Resumen:
In previous studies we have
demonstrated that atrial natriuretic peptide (ANP) increases vascular nitric oxide
synthase (NOS) activity in spontaneously hypertensive rats (SHR). The aim was
to study receptors, signaling pathways and NOS isoforms
involved in this interaction in aorta artery. NOS
activity (using L-[U14C]-arginina as substrate) induced by ANP (1uM) was
determined in presence of: inducible (iNOS)
and neuronal NOS (nNOS) inhibitors, cANP (4-23) (NPR-C natriuretic receptor
agonist), NPR-A/B natriuretic receptor antagonist, 8Br-cGMP (stable analogue of
cGMP), PKG, Gi protein and calmodulin inhibitors. Endotelial NOS (eNOS)
expression was determined by Western blot. Results: iNOS and nNOS blockade did
not modify NOS activity induced by ANP. The increase in NOS activity induced by
cANP was lower than the observed with ANP. NPR-A/B blockade partially decreased
ANP effect. NOS activation via ANP was totally inhibited by calmodulin
inhibition and it was blunted when PKG or Gi were blocked. 8-Br-cGMP partially
mimiked ANP effect. eNOS expression was not modified by ANP. Conclusion: ANP
would interact with NPRA/B activating cGMP/PKG signaling and with NPR-C
activating Gi protein. Through both pathways ANP would promote the activation
of Ca2+-calmodulin dependent eNOS in aorta artery of SHR. (ANOVA,
postest:Bonferroni)