Angiotensin-II Stimulates DNA Synthesis in rat adrenal zona glomerulosa cells: Receptor subtypes involved and possible signal transduction mechanism
| Autor: | Gastone G. Nussdorfer, Piera Rebuffat, Giuseppina Mazzocchi, Ludwik K. Malendowicz, Giuseppe Gottardo |
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| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty medicine.drug_class Biology Endocrinology Internal medicine medicine Animals Humans Rats Wistar Protein Kinase C Protein kinase C Receptors Angiotensin DNA synthesis Phospholipase C Angiotensin II DNA General Medicine Protein-Tyrosine Kinases Receptor antagonist Molecular biology Rats medicine.anatomical_structure Zona glomerulosa Zona Glomerulosa Signal transduction Tyrosine kinase Cell Division hormones hormone substitutes and hormone antagonists Signal Transduction |
| Zdroj: | Endocrine Research. 23:191-203 |
| ISSN: | 1532-4206 0743-5800 |
| DOI: | 10.3109/07435809709031853 |
| Popis: | Using an in situ perfusion technique of isolated left rat adrenal gland, it has been demonstrated that angiotensin-II (ANG-II) increases DNA synthesis in the zona glomerulosa (ZG), but not fasciculata-reticularis cells. The AT1 receptor antagonist DuP753 abolished the effect of ANG-II, while the AT2 receptor antagonist PD 123319 potentiated it. Both Ro31-8220, an inhibitor of protein kinase C (PKC), and tyrphostin-23, an inhibitor of tyrosine kinase (TK), evoked a partial reversal of ANG-II effect, and when added together to the perfusion medium abolished it. In contrast, the phospholipase C inhibitor U-73122 alone was able to induce a complete blockade of ANG-II effect. Neither the phospholipase A2 inhibitor AACOCF3 nor the cyclooxygenase inhibitor indomethacin and the lipoxygenase inhibitor phenidone affected ANG-II-induced stimulation of DNA synthesis, thereby making unlikely the involvement of the arachidonic acid signaling pathways. Our findings suggest that (i) ANG-II stimulates rat ZG cell proliferation acting via AT1 receptors coupled with phospholipase C, which activates both PKC and TK signaling systems; and (ii) the proliferogenic effect of ANG-II is partially counteracted by the activation of the AT2 receptor subtype. |
| Databáze: | OpenAIRE |
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