| Full text | |
| Author(s): |
Martinelli, Ariane Migliato
[1]
;
dos Santos Rodrigues, Carla Nascimento
[1]
;
de Moraes, Thiago Francisco
[1]
;
Rodrigues, Gerson Jhonatan
[1]
Total Authors: 4
|
| Affiliation: | [1] Univ Fed Sao Carlos, Dept Ciencias Fisiol, Sao Carlos, SP - Brazil
Total Affiliations: 1
|
| Document type: | Journal article |
| Source: | JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES; v. 21, p. 38-45, 2018. |
| Web of Science Citations: | 1 |
| Abstract | |
Purpose. In endothelial cells, investigate if the soluble guanylate cyclase (sGC) activation or stimulation is able to potentiate the relaxation in vessels. Methods. Aortic and coronary rings with and without endothelium were placed in a myograph and cumulative concentration-effect curves for DETA-NO or ataciguat were performed. Nitric oxide (NO) were measured by fluorescence or by selective electrode in human umbilical endothelial cells (HUVECs) in response to some treatments, including ataciguat, 8-Br-cGMP and A23187. Results. The presence of the endothelium potentiated the relaxation induced by DETANO in aortic and coronary rings. In addition, in aortic rings the endothelium potentiated the relaxation induced by ataciguat. In the presence of nitric oxide synthase (NOS) inhibitor, the endothelium effect was abolished to DETANO or ataciguat, in both vessels. Ataciguat, 8-Br-cGMP and A23187 were able to induce NO production in HUVECs cells. In the presence of NOS inhibitor, the NO production induced by ataciguat and 8-Br-cGMP was abolished. Conclusions. Our results suggest that in aortic and coronary rings the endothelium potentiates the relaxation induced by activation or stimulation of sGC through a mechanism dependent of NOS activation. (AU) | |
| FAPESP's process: | 12/24477-8 - Utilization of ruthenium complex as pharmacological strategy to revert and/or prevent the endothelial dysfunction |
| Grantee: | Gerson Jhonatan Rodrigues |
| Support Opportunities: | Research Grants - Young Investigators Grants |