| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo 14214; and 2 Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263
One of the major physiological regulators for the production and release of renin from the kidney is blood pressure. The juxtaglomerular (JG) cells, located primarily at the afferent arterioles leading to the glomerulus, are thought to be the baroreceptor of the kidney and adjust their ability to secrete renin in an inverse relationship to changes in pressure (mechanical force). The characteristics of JG cells that allow them to sense and respond to changes in mechanical force at the cellular level are not clear. By use of a renin-expressing clonal cell line (As4.1) as a model for JG cells, it was the purpose of this paper to identify cellular pathways that are activated by mechanical distension. Fura 2-labeled As4.1 cells were mechanically probed to observe changes of intracellular calcium concentration ([Ca2+]i). Mechanical distension of As4.1 cells resulted in an influx of Ca2+ to the cytosol, mediated by stretch-activated ion channels and dependent on the presence of extracellular Ca2+. Furthermore, cyclic mechanical distension elevated total inositol phosphates (IP) in As4.1 cells. This response was also dependent on the presence of extracellular Ca2+, and the addition of U-73122, a phospholipase C (PLC) antagonist, significantly attenuated the increase of IP. Taken together, these findings demonstrate the calcium-dependent activation of PLC and the subsequent increase of IP and [Ca2+]i to be a potentially important pathway for the modality of pressure sensing by renin-expressing cells in response to mechanical stimulation.
pressure; inositol phosphates; baroreceptors; signal transduction
This article has been cited by other articles:
|
|
 |
|
  L. Pan, Y. Wang, C. A. Jones, S. T. Glenn, H. Baumann, and K. W. Gross Enhancer-dependent inhibition of mouse renin transcription by inflammatory cytokines Am J Physiol Renal Physiol, January 1, 2005; 288(1): F117 - F124. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. G. Friis, F. Jorgensen, D. Andreasen, B. L. Jensen, and O. Skott Molecular and Functional Identification of Cyclic AMP-Sensitive BKCa Potassium Channels (ZERO Variant) and L-Type Voltage-Dependent Calcium Channels in Single Rat Juxtaglomerular Cells Circ. Res., August 8, 2003; 93(3): 213 - 220. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Gentil, C. Delphin, C. Benaud, and J. Baudier Expression of the Giant Protein AHNAK (Desmoyokin) in Muscle and Lining Epithelial Cells J. Histochem. Cytochem., March 1, 2003; 51(3): 339 - 348. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Ryan, T. A. Black, S. L. Millard, K. W. Gross, and G. Hajduczok Endothelin-1 increases calcium and attenuates renin gene expression in As4.1 cells Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2458 - H2465. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Ryan, T. A. Black, K. W. Gross, and G. Hajduczok Cyclic mechanical distension regulates renin gene transcription in As4.1 cells Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E830 - E837. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
