Bibliographic Details
| Title: |
Bradykinin/B2 receptor activation regulates renin in M-1 cells via protein kinase C and nitric oxide. |
| Authors: |
Lara, Lucienne S.1,2,3, Bourgeois, Camille R. T.2, El‐Dahr, Samir S.3,4, Prieto, Minolfa C.2,3 mprieto@tulane.edu |
| Source: |
Physiological Reports. Apr2017, Vol. 5 Issue 7, p1-N.PAG. 14p. |
| Subject Terms: |
*RENIN regulation, *BRADYKININ receptors, *MONOCYTES, *PROTEIN kinase C, *NITRIC oxide |
| Abstract: |
In the collecting duct (CD), the interactions of renin angiotensin system (RAS) and kallikrein-kinin system (KKS) modulate Na+ reabsorption, volume homeostasis, and blood pressure. In this study, we used a mouse kidney cortical CD cell line (M-1 cells) to test the hypothesis that in the CD, the activation of bradykinin B2 receptor (B2R) increases renin synthesis and release. Physiological concentrations of bradykinin (BK) treatment of M-1 cells increased renin mRNA and prorenin and renin protein contents in a dosedependent manner and increased threefold renin content in the cell culture media. These effects were mediated by protein kinase C (PKC) independently of protein kinase A (PKA) because B2R antagonism with Icatibant and PKC inhibition with calphostin C, prevented these responses, but PKA inhibition with H89 did not modify the effects elicited by the B2R activation. BK-dependent stimulation of renin gene expression in CD cells also involved nitric oxide (NO) pathway because increased cGMP levels and inhibition of NO synthase with L-NAME prevented it. Complementary renin immunohistochemical studies performed in kidneys from mice with conventional B2R knockout and conditional B2R knockout in the CD, showed marked decreased renin immunoreactivity in CD, regardless of the renin presence in juxtaglomerular cells in the knockout mice. These results indicate that the activation of B2R increases renin synthesis and release by the CD cells through PKC stimulation and NO release, which support further the interactions between the RAS and KKS. [ABSTRACT FROM AUTHOR] |
|
Copyright of Physiological Reports is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| Database: |
Academic Search Complete |
