The Korean Journal of Physiology and Pharmacology

  • 제21권6호
  • /
  • Pages.667-674
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  • 2017
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  • 1226-4512(pISSN)
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  • 2093-3827(eISSN)
대한약리학회 (The Korean Society of Pharmacology)
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Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats

  • Phuong, Hoang Thi Ai (Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School) ;
  • Yu, Lamei (Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School) ;
  • Park, Byung Mun (Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School) ;
  • Kim, Suhn Hee (Department of Physiology, Research Institute for Endocrine Sciences, Chonbuk National University Medical School)
  • 투고 : 2017.06.28
  • 심사 : 2017.08.07
  • 발행 : 2017.11.01
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초록

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 $1{\mu}M$) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) ($0.1{\mu}M$)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor ($AT_1R$) but not by an antagonist of $AT_2R$ or $AT_4R$. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate ($IP_3$) 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) $10{\mu}M$ 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 $AT_1R$ and $PLC/IP_3/PKC$ 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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참고문헌

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