Angiotensin III stimulates high stretch-induced ANP secretion via angiotensin type 2 receptor |
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| Affiliation: | 1. Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Republic of Korea;2. Internal Medicine, Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Republic of Korea;1. MOE Key Laboratory of Theoretical Chemistry of Environment, Center for Computational Quantum Chemistry, South China Normal University, Guangzhou 510631, China;2. Institute of Chemical Physics, Beijing Institute of Technology, Beijing 100081, China;3. School of Chemistry and Chemical Engineering, Shaanxi Normal University, Xi’an 710139, China;4. Department of Chemistry and Center for Computational Chemistry, University of Georgia, Athens, GA 30602, USA;1. PhD Program in Biological and Health Sciences, Universidad Autónoma Metropolitana (UAM) Iztapalapa-Xochimilco-Cuajimalpa, Mexico City, Mexico;2. Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla, Estado de México, Mexico;3. Department of Neurosciences, National Rehabilitation Institute “Luis Guillermo Ibarra Ibarra” (INR) Secretaría de Salud (SSA), Mexico City, Mexico;4. Departament of Reproductive Biology, Universidad Autónoma Metropolitana (UAM) Campus Iztapalapa, Mexico City, Mexico |
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| Abstract: | Angiotensin III (Ang III) is metabolized from Ang II by aminopeptidase (AP) A and in turn, Ang III is metabolized to Ang IV by APN. Ang III is known to have a similar effect to Ang II on aldosterone secretion, but the effect of Ang III on atrial natriuretic peptide (ANP) secretion from cardiac atria is not known. The aim of the present study is to define the effect of Ang III on ANP secretion and its receptor subtype using isolated perfused beating atria. The volume load was achieved by elevating the height of outflow catheter connected with isolated atria from 5 cmH2O to 7.5 cmH2O. Atrial stretch by volume load increased atrial contractility and ANP secretion. Ang III stimulated stretch-induced ANP secretion in a dose-dependent manner without change in atrial contractility. The stimulated effect of Ang III (1 μM) on stretch-induced ANP secretion was blocked by the pretreatment of Ang II type 2 (AT2) receptor antagonist but not by AT1 or Mas receptor antagonist. Pretreatment with inhibitor of phosphoinositide 3-kinase (PI3K), Akt, nitric oxide synthase, soluble guanylyl cyclase, or protein kinase G (PKG) attenuated Ang III-stimulated ANP secretion. When Ang III (40 nM) or Ang II (4 nM) was infused for 10 min into anesthetized rats, mean arterial pressure was increased about 10%. However, Ang III increased plasma ANP level by 35.81 ± 10.19% but Ang II decreased plasma ANP level by 30.41 ± 7.27%. Therefore, we suggest that Ang III, opposite to Ang II, stimulated stretch-induced ANP secretion through AT2 receptor/PI3K/Akt/nitric oxide/PKG pathway. |
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