Figure 4.

Characterization of renal responses in protein kinase Cα knock out mice. (a) Protein kinase C knock out mice were placed in metabolic cages, following acclimation period; urine volumes were obtained and electrolytes analyzed during normal chow and high salt feedings. Mice were challenged with a bolus of the sodium chloride cotransporter inhibitor (hydrochlorothiazide, 12.5 mg/BW Intraperitoneal) and urine volumes obtained for 12 h. Data are shown in mmol/day, normalized to 100 g total BW of each mouse. Data shown as mean ± SEM, n = 5–6, *P < 0.05, **P < 0.01, ***P < 0.001. Total protein was used for Western blot analysis of sodium chloride cotransporter in protein kinase C knock out and control mice were normal chow and high salt (4%, 12 days) feedings. (b) Protein expression of sodium chloride cotransporter is shown in protein kinase C knock out mouse cortex homogenates as compared to control mice following normal chow. (c) Protein expression of sodium chloride cotransporter is shown in protein kinase C knock out mouse cortex homogenates during low salt (<0.05%, 12 days) and high salt (4%, 12 days) feeding. (d) Protein expression of sodium chloride cotransporter is shown in protein kinase C knock out mouse cortex homogenates as compared with control mice following high salt feeding. (e) Protein expression of sodium chloride cotransporter is shown in protein kinase C knock out mouse cortex homogenates as compared with control mice following low salt feeding. Representative blots for each group are shown, along with loading control, GAPDH. Sodium chloride cotransporter band densities were normalized to GAPDH values and are shown in arbitrary units. Data are shown as mean ± SEM, n = 4–5, *P < 0.05, **P < 0.01. GAPDH, glyceraldehyde 3-phosphate dehydrogenase.