Juxtaglomerular cell activity during hemorrhage and ischemia as revealed by quinacrine histofluorescence

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Abstract
Quinacrine (QC) binds with high affinity to the intracellular storage granules of juxtaglomerular cells (JG-cells) in the afferent arteriolus of the glomerulus of the kidney. The release of QC bound to JG-cells was studied. The cells were stimulated by renal ischemia and hemorrhagic shock combined with immobilization stress. One hour after onset of renal ischemia QC-JGI in 14C-QC-treated rats decreased to .apprx. 40% in the ischemic kidney compared to a nonligated control kidney. The 14C-contents in the ischemic kidney decreased to 33% of that in the untouched control kidney. Hemorrhagic shock was obtained by bleeding into a reservoir for 15 min or 1 h. Rats who received QC or 14C-QC 1 h before onset of bleeding showed no change in QC-JGI (15 min shock) or 14C-contents (1 h shock) compared to controls. This was probably due to formation of new QC-binding granules, which binds circulating quinacrine thereby masking a release. If the time between the QC injection and the onset of shock was extended to .apprx. 15 h, when circulating amounts of QC are very low, a decrease of QC-JGI (.apprx. 30% of controls) was seen in the kidneys of the shocked rats. QC in vivo bound to granules of JG-cells could be released with the content of the granules following stimuli known to induce renin release. Quinacrine-binding may provide a new method to study endocrine cells in the way it has been used in the present study as a marker of JG-cell activity.