Role of Gap Junction in the Regulation of Renin Release and Intracellular Calcium in As 4.1 Cell Line.
- Author:
Jeong Hee HAN
1
;
Bing Zhe HONG
;
Young Geun KWAK
;
Kuichang YUAN
;
Woo Hyun PARK
;
Sung Zoo KIM
;
Suhn Hee KIM
Author Information
1. Department of Physiology, Chonbuk National University Medical School, Jeonju 561-180, Korea.
- Publication Type:Original Article
- Keywords:
As 4.1 cell line;
Ca2+;
Gap junction;
Hormone;
Renin
- MeSH:
Amiloride;
Calcium*;
Cell Line*;
Connexins;
Endothelial Cells;
Gap Junctions*;
Glycyrrhetinic Acid;
Heptanol;
Kidney;
Nifedipine;
Nimodipine;
Renin*;
Ryanodine;
Thapsigargin
- From:The Korean Journal of Physiology and Pharmacology
2007;11(3):107-112
- CountryRepublic of Korea
- Language:English
-
Abstract:
Gap junction protein, connexin, is expressed in endothelial cells of vessels, glomerulus, and renin secreting cells of the kidney. The purpose of this study was to investigate the role of gap junction in renin secretion and its underlying mechanisms using As 4.1 cell line, a renin-expressing clonal cell line. Renin release was increased proportionately to incubation time. The specific gap junction inhibitor, 18-beta glycyrrhetinic acid (GA) increased renin release in dose-dependent and time- dependent manners. Heptanol and octanol, gap junction blockers, also increased renin release, which were less potent than GA. GA-stimulated renin release was attenuated by pretreatment of the cells with amiloride, nifedipine, ryanodine, and thapsigargin. GA dose-dependently increased intracellular Ca2+ concentration, which was attenuated by nifedipine, nimodipine, ryanodine, and thapsigargin. However, RP-cAMP, chelerythrine, tyrphostin A23, or phenylarsine oxide did not induced any significant change in GA-stimulated increase of intracellular Ca2+ concentration. These results suggest that gap junction plays an important role on the regulation of renin release and intracellular Ca2+ concentration in As 4.1 cells.
