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KMID : 0811720170210060667
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Korean Journal of Physiology & Pharmacology
2017 Volume.21 No. 6 p.667 ~ p.674
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Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats
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Phuong Hoang Thi Ai
Yu La Mei
Park Byung-Mun
Kim Suhn-Hee
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Abstract
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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.
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KEYWORD
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Angiotensin-(4-8), Angiotensin II, Angiotensin type 1 receptor, Atrial natriuretic peptide, Heart, Signal pathway
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