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. 2020 Jul 13;319(3):F366–F379. doi: 10.1152/ajprenal.00501.2019

Fig. 4.

Fig. 4.

Adaptation of glutamine transporter and ammoniagenic enzymes in the kidney cortex of rats treated with acetazolamide (ACTZ) or NH4Cl loading for 6 days. A and D: tissue homogenates (enzymes) and membrane fractions (SNAT3) were isolated from the kidney cortex of rats treated with NH4Cl loading (A) or ACTZ (D) versus their respective control or vehicle treatment and were used for immunoblot analysis using specific antibodies for each protein. B, C, E, and F: corresponding average means ± SE of the densitometry analysis of SNAT3 (B and E) and ammoniagenic enzymes (C and F) in response to NH4Cl loading versus control (B and C) or in ACTZ-treated versus vehicle-treated rats (E and F). The abundance of these proteins was normalized to actin used for the control of gel loading. As shown, SNAT3, phosphate-dependent glutaminase (PGA), and glutamate dehydrogenase (GDH) were sharply upregulated in NH4Cl-loaded rats but not in ACTZ-treated rats. n = 5 rats in each group. Each lane was loaded with 10−30 μg protein from the kidney cortex. Note that the exposure time for SNAT3 in vehicle versus ACTZ (D) was much higher than that in control versus 6 days of NH4Cl loading (A). GS, glutamine synthetase; NS, not significant.