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First published online on April 15, 2005.
Experimental Physiology (2005)
DOI: 10.1113/expphysiol.2004.029611
© The Physiological Society 2005
A more recent version of this article appeared on July 1, 2005
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Received December 9, 2004
Revised January 26, 2005
Accepted after revision March 18, 2005

GI and epithelial physiology

Inhibition of the carbachol-evoked oscillatory currents by NO Donor Sodium Nitroprusside in guinea pig ileal myocytes

Seung-Soo Chung 1, Duck-Sun Ahn 1, Hong-Ghi Lee 1, Young-Ho Lee 1, Taick-Sang Nam 1*

1 Yonsei University

* To whom correspondence should be addressed. E-mail: tsnam{at}yumc.yonsei.ac.kr.


  Abstract
The effect of sodium nitroprusside (SNP) on carbachol (CCh)-evoked inward cationic current (Icat )oscillations in guiea pig ileal longitudinal myocytes were investigated using the whole cell patch-clamp technique and permeabilized preparation of longitudinal muscle strip. SNP (10 µìM) completely inhibited Icat oscillations evoked by 1 µìM CCh. 1H-(1,2,4)oxadiazole[4,3-a]quinoxaline-1-one (ODQ) (1 µìM) almost completely prevented the inhibitory effect of SNP on Icat oscillations. 8-bromo-guanosine 3',5'-cyclic monophosphate (8-Br-cGMP) (30 µìM) in the pipette solution completely abolished Icat oscillations. But Rp-8-Br-cGMP (30 µìM) in pipette solution significantly attenuated the inhibitory SNP effect on Icat oscillations. When [Ca2+]i was held to the resting level using 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) (10 mM) and Ca2+ (4.6 mM) in the pipette solution, CCh (1 µìM) evoked only the sustained component of Icat without any oscillations and SNP was without effect on this current. In the presence of a high concentration of inositol 1,4,5-trisphosphate (IP3) (30 µìM) in the patch pipette solutions, the inhibitory effect of SNP (10 µìM) on Icat oscillations was siginificantly prevented with the reduced frequency. SNP significantly inhibited the Ca2+ release evoked by either CCh or inositol 1,4,5-trisphosphate IP3, but not by caffeine in the permeabilized preparations of longitudinal muscle strip. The results suggest that inhibitory effects of SNP on Icat oscillations are mediated, in part, by functional modulation of the IP3 receptor, and neither by the inhibition of cationic channels themselves or by the muscarinic receptors in the plasma membrane. This inhibition seems to be mediated by an increased cGMP concentration in a PKG-dependent manner.

Key Words: Cation current, cGMP, Nitric oxide






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