Cellular mechanism of angiotensin II-induced atrial natriuretic peptide release in rat right atrial tissue
| Autor: | Alain Carayon, Hayet Soualmia, F. Masson, Christiane Barthélemy, Geneviè Maistre |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
chemistry.chemical_element Tetrazoles Calcium In Vitro Techniques 1-Sarcosine-8-Isoleucine Angiotensin II General Biochemistry Genetics and Molecular Biology Calcium in biology Losartan Rats Sprague-Dawley Atrial natriuretic peptide Internal medicine medicine Animals Diltiazem Heart Atria General Pharmacology Toxicology and Pharmaceutics Protein kinase C Protein Kinase C Calcium metabolism Chemistry Angiotensin II Biphenyl Compounds Imidazoles General Medicine Chromatography Ion Exchange Rats Endocrinology cardiovascular system hormones hormone substitutes and hormone antagonists Atrial Natriuretic Factor circulatory and respiratory physiology medicine.drug |
| Zdroj: | Life sciences. 58(19) |
| ISSN: | 0024-3205 |
| Popis: | This study presents an investigation of the mechanism of angiotensin II (Ang II)-induced atrial natriuretic peptide (ANP) release in superfused sliced right atria of rats. Ang II (0.1 microM) enhanced ANP release by 49%. This phenomenon was significantly blocked by (Sara1-Ileu 8) Ang II (1 microM) and losartan (0.1 microM). The use of neomycin (100 microM), a phospholipase-C inhibitor completely suppressed the effect of Ang II on ANP increase. To elucidate the intracellular mechanism of ANP released by Ang II, the role of protein kinase C (PKC) was determined by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and phorbol ester : 4-beta-phorbol 12-myristate-13-acetate (PMA). We observed that PMA (0.1 microM) stimulated ANP release whereas H-7 (10 microM), an inhibitor of PKC in the presence of Ang II, prevented ANP increase. The role of calcium was also evaluated with 8-(N-N-diethylamino)-ocytyl-3,4,5, trimethoxy-benzoate (TMB-8) (10 microM) and N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide (W-7) (10 microM), which completely inhibited ANP release by Ang II. Pre-treatment with diltiazem (10 microM), an antagonist of the Ca++ channel, did not prevent ANP increase due to Ang II, but A23187 (5 microM) enhanced ANP release by Ang II. These results suggest that PKC and intracellular calcium play an important role in ANP release under the influence of Ang II in rat atrial tissue. |
| Databáze: | OpenAIRE |
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