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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Exp Physiol. 2010 Dec 17;96(3):305–316. doi: 10.1113/expphysiol.2010.055038

Figure 1. Inhibition of K+-secretion by CaCCinh-A01.

Figure 1

Figure 1

Figure 1

A. Isc (see Methods) was measured in adjacent isolated mucosae without (solid line) or with (dashed line) CaCCinh-A01 [30μM] added to mucosal and serosal baths ~20min prior to adrenaline [5μM] stimulation (*). Isc was significantly different between control and CaCCinh-A01 treated for basal conditions prior to adrenaline addition (ΔIsc= +36.6±3.1μA/cm2, n=4, P<0.002), as well as at the 1st peak, 2nd peak, and steady-state plateau (Table 1). B. The action of CaCCinh-A01 [30μM] on Isc during adrenaline stimulation (adrIsc) was measured as in panel A with ICI-118551 [0.3μM] present to suppress transient positive Isc. C. Inhibitory responses of CaCCinh-A01 (●, n=4), GlyH-101 (▴, n=4), and NPPB (▿, n=3) for adrIsc were measured in adjacent mucosae with ICI-118551 [0.3μM], by cumulative increases from 1μM to 30μM during steady-state activation. Fits of Henri-Michaelis-Menton kinetics (single binding site) were made to the resulting concentration dependences of adrIsc: CaCCinhEC50=6.3±1.4μM, GlyHEC50=9.4±0.7μM, NPPBEC50=36±9μM, with each significantly different from the others (P<0.05).