Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats
The Korean Journal of Physiology and Pharmacology
;
: 667-674, 2017.
Article
Dans Anglais
| WPRIM
| ID: wpr-727947
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.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Peptides
/
Phospholipases
/
Pression sanguine
/
Protéine kinase C
/
Angiotensine-II
/
Angiotensines
/
Transduction du signal
/
Facteur atrial natriurétique
/
Récepteur de type 1 à l'angiotensine-II
/
Pression artérielle
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
The Korean Journal of Physiology and Pharmacology
Année:
2017
Type:
Article
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