PERSONAL DE APOYO
ELESGARAY Rosana
artículos
Título:
Signaling cascade that mediates endothelial nitric oxide synthase activation induced by atrial natriuretic peptide
Autor/es:
ELESGARAY ROSANA; CANIFFI CAROLINA; RODRÍGUEZ IERACE DANIELA; VISINTINI JAIME M. FLORENCIA; FELLET ANDREA; ARRANZ CRISTINA; COSTA MARÍA ÁNGELES
Revista:
REGULATORY PEPTIDES
Editorial:
ELSEVIER SCIENCE BV
Referencias:
Año: 2008 p. 130 - 134
ISSN:
0167-0115
Resumen:
Atrial natriuretic peptide (ANP) induces activation of nitric oxide-synthase (NOS). Aims: to identify the
isoform of NOS involved in ANP effects, to study whether ANP modifies NOS expression and to investigate the
signaling pathways and receptors involved in NOS stimulation. NOS activation induced by ANP would be
mediated by endothelial NOS (eNOS) since neuronal or inducible NOS inhibition did not alter ANP effect. The
peptide induced no changes in eNOS protein expression. NOS activity stimulated by ANP, in the kidney, aorta
and left ventricle, was partially abolished by the NPR-A/B antagonist, as well as PKG inhibition, but no
difference in atria was observed. 8-Br-cGMP partially mimicked the effect of ANP on NOS in all tissues. NOS
stimulation by ANP in atria disappeared when G protein was inhibited, but this effect was partial in the other
tissues. Calmodulin antagonist abolished NOS stimulation via ANP. Inhibition of the PLC, PKC or PI3 kinase/
Akt pathway failed to alter NOS activation induced by ANP.
ANP would activate eNOS in the aorta, heart and kidney without modifying the expression of the enzyme.
ANP would interact with NPR-C coupled via G proteins leading to the activation of Ca2+calmodulindependent
NOS in atria; while in ventricle, aorta and kidney, ANP could also interact with NPR-A/B,
increasing cGMP, which in turns activates PKG to stimulate eNOS.fies NOS expression and to investigate the
signaling pathways and receptors involved in NOS stimulation. NOS activation induced by ANP would be
mediated by endothelial NOS (eNOS) since neuronal or inducible NOS inhibition did not alter ANP effect. The
peptide induced no changes in eNOS protein expression. NOS activity stimulated by ANP, in the kidney, aorta
and left ventricle, was partially abolished by the NPR-A/B antagonist, as well as PKG inhibition, but no
difference in atria was observed. 8-Br-cGMP partially mimicked the effect of ANP on NOS in all tissues. NOS
stimulation by ANP in atria disappeared when G protein was inhibited, but this effect was partial in the other
tissues. Calmodulin antagonist abolished NOS stimulation via ANP. Inhibition of the PLC, PKC or PI3 kinase/
Akt pathway failed to alter NOS activation induced by ANP.
ANP would activate eNOS in the aorta, heart and kidney without modifying the expression of the enzyme.
ANP would interact with NPR-C coupled via G proteins leading to the activation of Ca2+calmodulindependent
NOS in atria; while in ventricle, aorta and kidney, ANP could also interact with NPR-A/B,
increasing cGMP, which in turns activates PKG to stimulate eNOS.2+calmodulindependent
NOS in atria; while in ventricle, aorta and kidney, ANP could also interact with NPR-A/B,
increasing cGMP, which in turns activates PKG to stimulate eNOS.