Role of Gap Junction in the Regulation of Renin Release and Intracellular Calcium in As 4.1 Cell Line
Role of Gap Junction in the Regulation of Renin Release and Intracellular Calcium in As 4.1 Cell Line
- Jeong Hee Han Bing-Zhe Hong Young Geun Kwak Kuichang Yuan Woo Hyun Park Sung Zoo Kim Suhn Hee Kim
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제11권 제3호
- 등재여부 : KCI등재
- 2007.01
- 107 - 112 (6 pages)
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 Ca<SUP>2+</SUP> concentration, which was attenuated by nifedipine, nimodipine, ryanodine, and thapsigargin. However, RP-cAMP, chelerythrine, tyrphostin A23, or phenylarsine oxide did not induced any signi</SUP>ficant 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 Ca<SUP>2+</SUP> concentration in As 4.1 cells.