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. 1998 Jul 21;95(15):9003–9008. doi: 10.1073/pnas.95.15.9003

Figure 7.

Figure 7

Inhibition of forskolin-stimulated renin release by 8-pCPT-cGMP in primary cultures of mouse JG cells. Shown are control (-) JG cells containing endogenous cGK (both I and II, see Fig. 6) and JG cells after infection with adenoviral vectors expressing either luciferase (lucif., control vector), cGK I, or cGK II. Control and infected cells were incubated for 24 h to allow expression of cGK. Then the JG cells were incubated −/+ 250 μM 8-pCPT-cGMP for 1 h and subsequently with −/+ 10 μM forskolin for a further 24 h before JG cells and media containing released renin were harvested separately for renin activity assay. Basal release of renin for untreated controls (-) averaged 0.9 μg AT I/h/100 μg cellular protein/20 h, corresponding to a fractional release of 24.3 ± 2.8% (mean ± SEM, n = 4) of total renin activity. Results are expressed as percentage of inhibition of renin release stimulated by forskolin. In all experiments, forskolin-stimulated renin release averaged 2.1 ± 0.4 (SD) -fold. Data shown are expressed as the mean ± SEM from four to six different experiments. ∗, P < 0.05 and ∗∗, P < 0.01, compared with control and luciferase vectors.