Copyright
©The Author(s) 2016.
World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 150-159
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.150
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.150
Figure 6 Post-receptor signal transduction for bradykinin-evoked increase in baseline increase in short-circuit current.
The BK-evoked Isc was suppressed in the presence of the PLC inhibitor U73122, the PKC inhibitor Bis-I, the calmodulin inhibitor W7, the calmdulin kinase II inhibitor KN-62 (10 μM), or the MAPK pathway inhibitor PD 98059 (eP < 0.01 vs BK alone). Inhibitor of PKA (KT5720 1 μM) or inhibitor of tyrosine protein kinase (genistein 10 μM) did not have a significant effect on BK-evoked increase in Isc. Isc: Increase in short-circuit current; BK: Bradykinin; PLC: Phospholipase C; PKC: Protein kinase C; Bis-I: Bisindolymaleimide I.
- Citation: Qu MH, Ji WS, Zhao TK, Fang CY, Mao SM, Gao ZQ. Neurophysiological mechanisms of bradykinin-evoked mucosal chloride secretion in guinea pig small intestine. World J Gastrointest Pathophysiol 2016; 7(1): 150-159
- URL: https://www.wjgnet.com/2150-5330/full/v7/i1/150.htm
- DOI: https://dx.doi.org/10.4291/wjgp.v7.i1.150