Academic Journal
Pharmacological properties of the Ca 2+ ‐release mechanism sensitive to NAADP in the sea urchin egg
| العنوان: | Pharmacological properties of the Ca 2+ ‐release mechanism sensitive to NAADP in the sea urchin egg |
|---|---|
| المؤلفون: | Genazzani, A A, Mezna, M, Dickey, D M, Michelangeli, F, Walseth, T F, Galione, A |
| المصدر: | British Journal of Pharmacology ; volume 121, issue 7, page 1489-1495 ; ISSN 0007-1188 1476-5381 |
| بيانات النشر: | Wiley |
| سنة النشر: | 1997 |
| المجموعة: | Wiley Online Library (Open Access Articles via Crossref) |
| الوصف: | The sea urchin egg homogenate is an ideal model to characterize Ca 2+ ‐release mechanisms because of its reliability and high signal‐to‐noise‐ratio. Apart from the InsP 3 ‐ and ryanodine‐sensitive Ca 2+ ‐release mechanisms, it has been recently demonstrated that this model is responsive to a third independent mechanism, that has the pyridine nucleotide, nicotinic acid adenine dinucleotide phosphate (NAADP), as an endogenous agonist. The sea urchin egg homogenate was used to characterize the pharmacological and biochemical characteristics of the novel Ca 2+ ‐releasing agent, NAADP, compared to inositol trisphosphate (InsP 3 ) and cyclic ADP ribose (cyclic ADPR), an endogenous activator of ryanodine receptors. NAADP‐induced Ca 2+ ‐release was blocked by L‐type Ca 2+ ‐channel blockers and by Bay K 8644, while InsP 3 ‐ and cyclic ADPR‐induced Ca 2+ ‐release were insensitive to these agents. L‐type Ca 2+ ‐channel blockers did not displace [ 32 P]‐NAADP binding, suggesting that their binding site was different. Moreover, stopped‐flow kinetic studies revealed that these agents blocked NAADP in a all‐or‐none fashion. Similarly, a number of K + ‐channel antagonists blocked NAADP‐induced Ca 2+ ‐release selectively over InsP 3 ‐ and cyclic ADPR‐induced Ca 2+ ‐release. Radioligand studies showed that these agents were not competitive antagonists. As has been shown for InsP 3 and ryanodine receptors, NAADP receptors were sensitive to calmodulin antagonists, suggesting that this protein could be a common regulatory feature of intracellular Ca 2+ ‐release mechanisms. The presence of K + was not essential for NAADP‐induced Ca 2+ ‐release, since substitution of K + with other monovalent cations in the experimental media did not significantly alter Ca 2+ release by NAADP. On the contrary, cyclic ADPR and InsP 3 ‐sensitive mechanisms were affected profoundly, although to a different extent depending on the monovalent cation which substituted for K + . Similarly, modifications of the pH in the experimental media from 7.2 to 6.7 or ... |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1038/sj.bjp.0701295 |
| الاتاحة: | http://dx.doi.org/10.1038/sj.bjp.0701295 https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1038%2Fsj.bjp.0701295 https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1038/sj.bjp.0701295 |
| Rights: | http://onlinelibrary.wiley.com/termsAndConditions#vor |
| رقم الانضمام: | edsbas.3AFBAC3D |
| قاعدة البيانات: | BASE |
| DOI: | 10.1038/sj.bjp.0701295 |
|---|