IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
artículos
Título:
Role of nitric oxide as a key mediator on cardiovascular actions of atrial
Autor/es:
MARÍA A. COSTA, ROSANA ELESGARAY, CAROLINA CANIFFI, ANDREA FELLET, MYRIAM MAC LAUGHLIN,
Revista:
American journal of physiology. Heart and circulatory physiology
Editorial:
American Physiological Society
Referencias:
Lugar: United States ; Año: 2009
ISSN:
1522-1539
Resumen:
Role of nitric oxide as a key mediator on cardiovascular actions of atrial natriuretic peptide in spontaneously hypertensive rats.
Am J Physiol Heart Circ Physiol 298: H778H786, 2010. First published September 25, 2009; doi:10.1152/ajpheart.00488.2009.
The objective was to study atrial natriuretic peptide (ANP) effects on
mean arterial pressure (MAP) and cardiovascular nitric oxide (NO)
system in spontaneously hypertensive rats (SHRs), investigating the
receptors and signaling pathways involved. In vivo, SHRs and Wistar-
Kyoto (WKY) rats were infused with saline (0.05 ml/min) or ANP
(0.2 g·kg1·min1) for 1 h. MAP and nitrites and nitrates excretion
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
The objective was to study atrial natriuretic peptide (ANP) effects on
mean arterial pressure (MAP) and cardiovascular nitric oxide (NO)
system in spontaneously hypertensive rats (SHRs), investigating the
receptors and signaling pathways involved. In vivo, SHRs and Wistar-
Kyoto (WKY) rats were infused with saline (0.05 ml/min) or ANP
(0.2 g·kg1·min1) for 1 h. MAP and nitrites and nitrates excretion
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
The objective was to study atrial natriuretic peptide (ANP) effects on
mean arterial pressure (MAP) and cardiovascular nitric oxide (NO)
system in spontaneously hypertensive rats (SHRs), investigating the
receptors and signaling pathways involved. In vivo, SHRs and Wistar-
Kyoto (WKY) rats were infused with saline (0.05 ml/min) or ANP
(0.2 g·kg1·min1) for 1 h. MAP and nitrites and nitrates excretion
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
298: H778H786, 2010. First published September 25, 2009; doi:10.1152/ajpheart.00488.2009.
The objective was to study atrial natriuretic peptide (ANP) effects on
mean arterial pressure (MAP) and cardiovascular nitric oxide (NO)
system in spontaneously hypertensive rats (SHRs), investigating the
receptors and signaling pathways involved. In vivo, SHRs and Wistar-
Kyoto (WKY) rats were infused with saline (0.05 ml/min) or ANP
(0.2 g·kg1·min1) for 1 h. MAP and nitrites and nitrates excretion
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gi
g·kg1·min1) for 1 h. MAP and nitrites and nitrates excretion
(NOx) were determined. NO synthase (NOS) activity and endothelial
(eNOS), neuronal (nNOS) and inducible (iNOS) NOS expression
were measured in the heart and aorta. In vitro, heart and aortic NOS
activity induced by ANP was determined in the presence of iNOS and
nNOS inhibitors, natriuretic peptide receptor (NPR)-A/B blocker, Gii
protein, and calmodulin inhibitors. As a result, ANP diminished MAP
and increased NOx in both groups. Cardiovascular NOS activity was
higher in SHRs than in WKY rats. ANP increased NOS activity, but
the activation was lower in SHRs than in WKY rats. ANP had no
effect on NOS isoform expression. NOS activity induced by ANP was
not modified by iNOS and nNOS inhibitors. NPR-A/B blockade
blunted NOS stimulation via ANP in ventricle and aorta but not in
atria. Cardiovascular NOS response to ANP was reduced by Gii
protein and calmodulin inhibitors in both groups. In conclusion, in
atria, ventricle, and aorta, ANP interacts with NPR-C receptors,
activating Ca2-calmodulin eNOS through Gi protein. In ventricle
and aorta, NOS activation also involves NPR-A/B. The NOS response
to ANP was impaired in heart and aorta of SHRs. The impaired
NO-system response to ANP in hypertensive animals, involving
alterations in the signaling pathway, could participate in the maintenance
of high blood pressure in this model of hypertension.
and aorta, NOS activation also involves NPR-A/B. The NOS response
to ANP was impaired in heart and aorta of SHRs. The impaired
NO-system response to ANP in hypertensive animals, involving
alterations in the signaling pathway, could participate in the maintenance
of high blood pressure in this model of hypertension.
and aorta, NOS activation also involves NPR-A/B. The NOS response
to ANP was impaired in heart and aorta of SHRs. The impaired
NO-system response to ANP in hypertensive animals, involving
alterations in the signaling pathway, could participate in the maintenance
of high blood pressure in this model of hypertension.
2-calmodulin eNOS through Gi protein. In ventricle
and aorta, NOS activation also involves NPR-A/B. The NOS response
to ANP was impaired in heart and aorta of SHRs. The impaired
NO-system response to ANP in hypertensive animals, involving
alterations in the signaling pathway, could participate in the maintenance
of high blood pressure in this model of hypertension.