Endocrinology, Vol 131, 1588-1594, Copyright © 1992 by Endocrine Society

ARTICLES

Effects of angiotensin converting enzyme inhibition, sodium depletion, calcium, isoproterenol, and angiotensin II on renin secretion by individual renocortical cells

KM Geary, MK Hunt, MJ Peach, RA Gomez and RM Carey
Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville 22908.

Angiotensin-converting enzyme inhibition with enalapril increases the number of glomeruli with juxtaglomerular cells and the number of cells in the afferent arteriole that express the renin gene and contain renin. However, renin release from these newly recruited renin- containing cells has not been demonstrated. Sodium depletion also has been shown to increase renal renin messenger RNA levels. The aim of these studies was to determine whether increases in renin secretion are a result of altered numbers of cells synthesizing/releasing renin or a change in the amount of renin release per cell, or both. Adult Wistar- Kyoto rats were treated with enalapril or sodium depleted and single cell renin secretion of enzymatically dispersed renal cortical cells was examined by reverse hemolytic plaque assay. Enalapril treatment increased the number of renin secreting cells by approximately 10-fold (P < 0.05). The newly recruited renin-secreting cells were not responsive to changes in extracellular calcium concentration or the presence of isoproterenol. At physiological (2.5 mM) extracellular calcium concentration, the amount of renin secreted per cell was approximately 2-fold greater (P < 0.05) when cells from enalapril- treated rats were compared to controls and sodium depletion increased both the number of renin-secreting cells and the amount of renin secreted by approximately 35% (P < 0.05). Angiotensin II (AII) inhibited the number of cells secreting renin in cortical cells prepared from enalapril-treated and control rats. In conclusion, angiotensin converting enzyme inhibition increased renin secretion predominantly by recruitment of additional renin-secreting cells and, to a lesser extent, by augmentation of the amount of renin released per cell. In contrast, sodium depletion increased renin secretion equally by both mechanisms. Newly recruited renin-secreting cells were not regulated by the extracellular calcium concentration or beta-adrenergic stimulation. Angiotensin II inhibited renin secretion directly by decreasing the number of individual cells releasing renin through a process which was independent of the extracellular calcium concentration.

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