Am J Physiol Cell Physiol AJP: Heart and Circulatory Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 257: C596-C600, 1989;
0363-6143/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cole, W. C.
Right arrow Articles by Sanders, K. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cole, W. C.
Right arrow Articles by Sanders, K. M.

AJP - Cell Physiology, Vol 257, Issue 3 C596-C600, Copyright © 1989 by American Physiological Society

ARTICLES

G proteins mediate suppression of Ca2+-activated K current by acetylcholine in smooth muscle cells

W. C. Cole and K. M. Sanders
Department of Physiology, University of Nevada School of Medicine, Reno 89557.

The role of G proteins in cholinergic suppression of Ca2+-activated K current was studied in isolated canine colonic myocytes with the whole cell voltage-clamp technique. Acetylcholine (ACh; 10.0 microM) caused a 64 +/- 2.4% depression in the Ca2+-dependent component of the outward current evoked at potentials between -45 and -15 mV when GTP (0.1 microM) was included in the pipette-filling solution. This effect was reversed within 2-4 min on washout of ACh. Without GTP in the filling solution, ACh caused a 15 +/- 2.5% depression in outward current in 60% of the cells tested. When the non-hydrolyzable GTP analogues, GTP gamma S (0.1 mM) or 5'-guanylylimidodiphosphate (GppNHp; 0.1 mM) were used, the decrease in outward current was greater (85 +/- 4.2 and 78 +/- 6.5%, respectively), and it was not reversed on withdrawal of ACh. Dialysis of the cell interior with pipette solution containing pertussis toxin (1 ng/ml) for 30 min had no effect on the whole cell currents evoked on depolarization, but it abolished the effect of ACh on Ca2+-dependent outward current. These data suggest that coupling of muscarinic receptors to the inhibition of Ca2+-activated K channels is mediated by pertussis toxin-sensitive G proteins in colonic smooth muscle cells. G protein-mediated inhibition is distinctly different from the opening of muscarinic-regulated K channels in other cell types.


This article has been cited by other articles:


Home page
 Am. J. Respir. Crit. Care Med.Home page
H. KUME and K. TAKAGI
Inhibition of beta -Adrenergic Desensitization by KCa Channels in Human Trachealis
Am. J. Respir. Crit. Care Med., February 1, 1999; 159(2): 452 - 460.
[Abstract] [Full Text]

Home page
 Physiol. Rev.Home page
H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE
Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels
Physiol Rev, July 1, 1998; 78(3): 811 - 920.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
X.-m. Xia, B. Hirschberg, S. Smolik, M. Forte, and J. P. Adelman
dSLo Interacting Protein 1, a Novel Protein That Interacts with Large-Conductance Calcium-Activated Potassium Channels
J. Neurosci., April 1, 1998; 18(7): 2360 - 2369.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online