Abstract
Background Cardiac hypertrophy is an adaptive response of the heart to many cardio-vascular disorders including hypertension, infarction and defects of the valves. Elevated levels of cardiac cyclic guanosine-3',5'-monophosphate (cGMP) activate cGMP-dependent protein kinase I (cGKI), which reportedly exhibited either anti-fibrotic and anti-hypertrophic effects or did not change the cardiac remodeling response. Based on these conflicting results, we and others suggested that the ability of natriuretic peptides (NP) to oppose detrimental changes via cGMP/cGKI might be strongly influenced by the stress stimuli that actually trigger the harmful events i.e. Angiotensin II (Ang II) modulating multiple reno-vascular and cardiac functions via G q-coupled Ang II type 1 receptors (AT1Rs). It is the overall aim of this study to dissect the molecular details underlying the cross-talk between the NP/cGMP/cGKI pathway and AngII/AT1R signaling in the heart.
Highlights
Cardiac hypertrophy is an adaptive response of the heart to many cardio-vascular disorders including hypertension, infarction and defects of the valves
Elevated levels of cardiac cyclic guanosine-3',5'-monophosphate activate cGMP-dependent protein kinase I, which reportedly exhibited either anti-fibrotic and anti-hypertrophic effects or did not change the cardiac remodeling response. Based on these conflicting results, we and others suggested that the ability of natriuretic peptides (NP) to oppose detrimental changes via cGMP/cGKI might be strongly influenced by the stress stimuli that trigger the harmful events i.e. Angiotensin II (Ang II) modulating multiple reno-vascular and cardiac functions via G q-coupled Ang II type 1 receptors (AT1Rs)
It is the overall aim of this study to dissect the molecular details underlying the cross-talk between the NP/cGMP/cGKI pathway and AngII/AT1R signaling in the heart
Summary
Cardiac hypertrophy is an adaptive response of the heart to many cardio-vascular disorders including hypertension, infarction and defects of the valves. Elevated levels of cardiac cyclic guanosine-3',5'-monophosphate (cGMP) activate cGMP-dependent protein kinase I (cGKI), which reportedly exhibited either anti-fibrotic and anti-hypertrophic effects or did not change the cardiac remodeling response. Based on these conflicting results, we and others suggested that the ability of natriuretic peptides (NP) to oppose detrimental changes via cGMP/cGKI might be strongly influenced by the stress stimuli that trigger the harmful events i.e. Angiotensin II (Ang II) modulating multiple reno-vascular and cardiac functions via G q-coupled Ang II type 1 receptors (AT1Rs). It is the overall aim of this study to dissect the molecular details underlying the cross-talk between the NP/cGMP/cGKI pathway and AngII/AT1R signaling in the heart
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