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      Angiotensin II-induced phosphoinositide production and atrial natriuretic peptide release in rat atrial tissue.

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          Abstract

          The effect of angiotensin II (Ang II) on inositol phosphate (IP) production and atrial natriuretic peptide (ANP) release was studied in sliced rat atrial tissue. The ability of Ang II (10(-7) M) to stimulate IP accumulation was detected after 1 min of incubation, and the maximal increase was observed at 5 min. In (2-3H) inositol-labeled atrial tissue, Ang II induced the formation of (2-3H) inositol monophosphate (IP1) in a dose-dependent manner. The effect of Ang II (10(-7) M) on IP1 was prevented by losartan (10(-7) M) but was not affected by PD123319 (10(-7) M). Similar effects were observed on Ang II-induced ANP release in the presence of these antagonists. The mechanism of ANP liberation induced by this peptide was independent of cyclic adenosine monophosphate (cAMP) and regulated by nitric oxide (NO). The role of Ca2+ in the effect of Ang II was tested by 1,2-bis (o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM; 10(-5) M), a chelator of intracellular Ca2+ that prevented the release of ANP by Ang II stimulation. We concluded that Ang II induced IP production and ANP release through AT1 receptors. Stimulation of ANP release by Ang II was dependent on intracellular Ca2+.

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          Author and article information

          Journal
          J Cardiovasc Pharmacol
          Journal of cardiovascular pharmacology
          Ovid Technologies (Wolters Kluwer Health)
          0160-2446
          0160-2446
          May 1997
          : 29
          : 5
          Affiliations
          [1 ] Service de Biochimie Médicale, CHU Pitié-Salpêtrière, Paris, France.
          Article
          10.1097/00005344-199705000-00007
          9213202
          34306b81-e360-4d2e-9280-b5f7755b501a
          History

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