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

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 present study tests whether QC bound to JG-cells can be released. The cells were stimulated by renal ischemia and hemorrhagic shock combined with immobilization stress. 1 h after onset of renal ischemia QC-JGI (modified Hartroft & Hartroft 1953) in 14C-QC-treated rats had decreased to about 40% in the ischemic kidney compared to a not ligated control kidney. The 14C-contents in the ischemic kidney had 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) as compared to controls. This was probably due to formation of new QC-binding granules, which took up still circulating quinacrine thereby masking a release. If the time between the QC injection and the onset of shock was extended to about 15 h, when circulating amounts of QC are very low, a decrease of QC-JGI (about 30% of controls) was seen in the kidneys of the shocked rats. The results are compatible with the possibility that QC in vivo bound to granules of JG-cells could be released together with the content of the granules following stimuli known to induce renin release. Quinacrine-binding therefore possibly provides 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.