Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats.
10.4196/kjpp.2017.21.6.667
- Author:
Hoang Thi Ai PHUONG
1
;
Lamei YU
;
Byung Mun PARK
;
Suhn Hee KIM
Author Information
1. Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju 54907, Korea. shkim@chonbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Angiotensin-(4-8);
Angiotensin II;
Angiotensin type 1 receptor;
Atrial natriuretic peptide;
Heart;
Signal pathway
- MeSH:
Aminopeptidases;
Angiotensin II*;
Angiotensins*;
Animals;
Arterial Pressure;
Atrial Natriuretic Factor*;
Blood Pressure*;
Heart;
Hemodynamics;
Inositol;
Peptides;
Phospholipases;
Protein Kinase C;
Rats*;
Receptor, Angiotensin, Type 1;
Signal Transduction
- From:The Korean Journal of Physiology and Pharmacology
2017;21(6):667-674
- CountryRepublic of Korea
- Language:English
-
Abstract:
Angiotensin II (Ang II) is metabolized from N-terminal by aminopeptidases and from C-terminal by Ang converting enzyme (ACE) to generate several truncated angiotensin peptides (Angs). The truncated Angs have different biological effects but it remains unknown whether Ang-(4-8) is an active peptide. The present study was to investigate the effects of Ang-(4-8) on hemodynamics and atrial natriuretic peptide (ANP) secretion using isolated beating rat atria. Atrial stretch caused increases in atrial contractility by 60% and in ANP secretion by 70%. Ang-(4-8) (0.01, 0.1, and 1 µM) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) (0.1 µM)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor (AT₁R) but not by an antagonist of AT₂R or AT₄R. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate (IP₃) receptor, or nonspecific protein kinase C (PKC). The potency of Ang-(4-8) to inhibit ANP secretion was similar to Ang II. However, Ang-(4-8) 10 µM caused an increased mean arterial pressure which was similar to that by 1 nM Ang II. Therefore, we suggest that Ang-(4-8) suppresses high stretch-induced ANP secretion through the AT₁R and PLC/IP₃/PKC pathway. Ang-(4-8) is a biologically active peptide which functions as an inhibition mechanism of ANP secretion and an increment of blood pressure.
