Fig. 3.

FP mediates renin expression in the kidney. (A) In situ hybridization for FP in mouse kidney sections (10 μm) by using ³⁵S-labeled antisense cRNA probe (red). (Scale bar: 200 μm.) (B) FP mRNA expression detected by RT-PCR in microdissected mouse nephron segments. Controls without addition of reverse transcriptase (RT−) to show no PCR contamination: CCD, proximal convoluted tubule (PCT), preglomerular arteriole (PGA), glomerulus (Glom), and positive control (kidney cortex). (C) Visualization of renin granules in microdissected renal arterial vessels from WT and FP^−/− mice. Glomeruli are sheared off in the microdissection process. High-contrast regions, usually seen at the end of the afferent arterioles, represent clusters of renin-positive cells (red arrows), or renin-negative cells (green arrows). (D) Quantification of juxtaglomerular granular (JG) negative and positive afferent arterioles. (E) Effects of latanoprost (Lata), travoprost (Trav), and cicaprost (Cica) on renin mRNA expression in JG-enriched cultured cells. Both FP agonists (latanoprost and travoprost) stimulated an increase in renin mRNA expression in a dose-dependent manner in the WT group, and no effect was observed in FP^−/− mice. Each point represents mean ± SEM of 4 cell groups, repeated 3 times. *, P < 0.05 by one-way ANOVA test.