Angiotensin II-induced phosphoinositide production and atrial natriuretic peptide release in rat atrial tissue
Autor: | F. Masson, Joëlle Eurin, Geneviève Maistre, Christiane Barthélemy, Alain Carayon, Hayet Soualmia |
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Rok vydání: | 1997 |
Předmět: |
medicine.medical_specialty
Radioimmunoassay Peptide hormone In Vitro Techniques Phosphatidylinositols Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Atrial natriuretic peptide GTP-Binding Proteins Internal medicine medicine Cyclic AMP Animals Vasoconstrictor Agents Cyclic adenosine monophosphate Heart Atria Inositol phosphate Chelating Agents Pharmacology chemistry.chemical_classification Angiotensin II receptor type 1 Angiotensin II Myocardium Heart Cyclic AMP-Dependent Protein Kinases Stimulation Chemical Rats Endocrinology Losartan chemistry cardiovascular system Calcium Cardiology and Cardiovascular Medicine hormones hormone substitutes and hormone antagonists Atrial Natriuretic Factor medicine.drug |
Zdroj: | Journal of cardiovascular pharmacology. 29(5) |
ISSN: | 0160-2446 |
Popis: | 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+. |
Databáze: | OpenAIRE |
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