Korean J Physiol Pharmacol.  2007 Jun;11(3):107-112.

Role of Gap Junction in the Regulation of Renin Release and Intracellular Calcium in As 4.1 Cell Line

• Han JH
• Hong BZ
• Kwak YG
• Yuan K
• Park WH
• Kim SZ
• Kim SH

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.

Keyword

As 4.1 cell line; Ca2+; Gap junction; Hormone; Renin

MeSH Terms

Amiloride
Calcium*
Cell Line*
Connexins
Endothelial Cells
Gap Junctions*
Glycyrrhetinic Acid
Heptanol
Kidney
Nifedipine
Nimodipine
Renin*
Ryanodine
Thapsigargin
Amiloride
Calcium
Connexins
Glycyrrhetinic Acid
Heptanol
Nifedipine
Nimodipine
Renin
Ryanodine
Thapsigargin