1. Down-regulation of L-type calcium channels in inflamed circular smooth muscle cells of the canine colon 
Xiaorong Liu, Nancy J. Rusch, Joerg Striessnig, Sushil K. Sarna 
Gastroenterology 
Volume 120, Issue 2, Pages (February 2001)
DOI: /gast
Copyright © 2001 American Gastroenterological Association Terms and Conditions

2. Fig. 1
(A) Comparison of the expression of the α1C-subunit in circular smooth muscle membranes from normal (lanes 1 and 2) and inflamed (lanes 3 and 4) colon. Each lane was loaded with 10 μg protein. The density of the 200–240-kilodalton doublet bands corresponding to the long and short forms of the α1C-subunit was reduced in inflamed compared with normal colon. (B) Bar graph showing averaged data of Western blots comparing α1C-subunit expression between normal and inflamed colons (n = 4). (C) Immunoblot of the L-type Ca2+ channel α1C-subunit in circular smooth muscle cell membranes from normal canine colon. Both lanes were loaded with 10 μg protein. In the first lane, the α1C-subunit was recognized by the antibody (Ab) as a 200–240-kilodalton doublet immunoreactive band in the absence of the antigenic competing peptide (Ab −CP). No band was detected in the second lane when the antibody was incubated with the competing peptide (Ab +CP). The CP concentration was 1 μmol/L. (D) Comparison of the expression of the α-subunit of BKCa channels in circular smooth muscle membrane from normal (lanes 1 and 2) and inflamed (lanes 3 and 4) colon. Each lane was loaded with 10 μg protein. The density of the 125-kilodalton band was not different between normal and inflamed colon.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

3. Fig. 2
Whole-cell Ca2+ channel currents in circular smooth muscle cells of (A) normal and (B) inflamed canine colon. Control currents (top traces) were elicited by incremental 10-mV depolarizing steps from –80 to +60 mV in drug-free recording solutions and were blocked by 1 μmol/L nifedipine. The amplitude of control current was less in the inflamed cell. Cell capacitance values were 77.9 pF (normal cell) and 73.1 pF (inflamed cell).
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

4. Fig. 3
(A) Current-voltage relationships comparing peak Ca2+ current density between circular smooth muscle cells from normal and inflamed colon. The density was significantly suppressed in the inflamed cells. (B) Analysis of normalized peak Ca2+ current densities reveals overlapping I-V relationships, implying similar activation and sensitivity voltages for Ca2+ channels in normal and inflamed cells. Peak Ca2+ current density was significantly less (*P < 0.05) in inflamed than normal cells at the indicated membrane potential. Sample sizes for normal and inflamed cells were 17 and 18, respectively.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

5. Fig. 4
Whole-cell Ca2+ channel currents in circular smooth muscle cells of (A) normal and (B) inflamed canine colon. The control currents (top traces) elicited by incremental 10-mV depolarizing steps from −80 to +60 mV were suppressed in the inflamed compared with the normal cell, but current was proportionally increased by 1 μmol/L Bay K 8644 in both preparations. Cell capacitance values were 78.2 pF (normal cell) and 73.5 pF (inflamed cell).
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

6. Fig. 5
I-V relationships demonstrating the agonist effect of 1 μmol/L Bay K 8644 on peak Ca2+ channel current density in (A) normal and (B) inflamed circular smooth muscle cells, respectively. Inflamed cells showed less control Ca2+ channel current density than normal cells, but both cell preparations showed proportional increases to Bay K Peak Ca2+ channel current density in the presence of Bay K 8644 was significantly higher (*P < 0.05) than in control solution at the indicated membrane potential. Sample sizes for normal and inflamed cells, n = 6.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

7. Fig. 6
Whole-cell Ca2+ channel currents in circular smooth muscle cells of (A) normal and (B) inflamed canine colon. The control currents (top traces) elicited by incremental 10-mV depolarizing steps from –80 to +60 mV were suppressed in the inflamed compared with the normal cell. Addition of 30 μmol/L acetylcholine (ACh) increased the level of Ca2+ current in the normal cell, whereas Ca2+ channel current in the inflamed cell did not respond to this cholinergic agonist. Cell capacitance values were pF (normal cell) and pF (inflamed cell).
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

8. Fig. 7
Current-voltage relationships demonstrating the effect of 30 μmol/L acetylcholine (ACh) on peak Ca2+ current density in (A) normal and (B) inflamed circular smooth muscle cells, respectively. The control Ca2+ current density in normal cells was enhanced by ACh, whereas inflamed cells showed a suppressed Ca2+ current density and did not respond to ACh. Peak current density in the presence of ACh was significantly higher (*P < 0.05) than in control solution at the indicated membrane potential. Sample sizes for normal and inflamed cells were 5 and 6, respectively.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions