. 2020 Mar 10;21(5):1887. doi: 10.3390/ijms21051887

Table 2.

Basic SCC and responses to in vitro pharmacological interventions.

Baseline	UC (µA · cm⁻²)		Controls (µA · cm⁻²)		p value
Baseline	107.6 ± 8.6 ^a		107.5 ± 16.7 ^a		0.99
ENaC inhibition	−35.1 ± 7.5 ^b		−37.2 ± 8.4 ^b		0.85
Baseline after ENaC inhibition	70.8 ± 7.5 ^a		66.0 ± 14.4 ^a		0.77
Non-specific PDE inhibition	22.0 ± 3.7 ^b		23.8 ± 5.2 ^b		0.77
COX-1 inhibition	−31.3 ± 3.8 ^b		−26.2 ± 4.7 ^b		0.40
COX-2 inhibition	−51.6 ± 10.5 ^b		−21.0 ± 3.7 ^b		*0.01*
PGE₂ concentration response	EC₅₀ (nM)	R_max (µA cm⁻²)	EC₅₀ (nM)	R_max (µA cm⁻²)	EC₅₀ (nM)	R_max
High-affinity receptor	14.2 ± 2.7	60.9 ± 5.8	11.0 ± 2.4	52.1 ± 6.9	0.39	0.34
Low-affinity receptor	588.8 ± 106.7	83.1 ± 11.2	493.2 ± 110.6	84.7 ± 13.4	0.54	0.93

First row shows baseline short-circuit current (SCC) measured 10 min after mounting (UC: n = 33, controls: n = 15). Second row: inhibition of ENaC mediated sodium absorption induces a decrease in SCC (UC: n = 32, controls: n = 15). Third row: after ENaC inhibition, the new baseline SCC is driven by anion secretion. Fourth row: SCC increase after non-specific PDE inhibition (UC: n = 31, controls: n = 11). Rows five and six show SCC response (decrease) to COX-1 (UC: n = 27, controls: n = 12) and COX-2 inhibition (UC: n = 28, controls: n = 11), respectively. Rows seven and eight include half maximal effective concentration (EC₅₀) and maximal receptor response (R_max) of a high- and a low-affinity PGE₂ receptor (UC: n = 19, controls: n = 12). SCC is recorded as µA · cm⁻². n = number of patients included in experiment. Due to unstable and/or non-vital biopsies after mounting in MUAS chambers, not all patients are represented in this section. ^a Data are shown as mean SCC ± SEM. ^b Data are shown as mean ∆SCC ± SEM.