AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 281: G1238-G1245, 2001;
0193-1857/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (11)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Murthy, K. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murthy, K. S.
Vol. 281, Issue 5, G1238-G1245, November 2001

cAMP inhibits IP3-dependent Ca2+ release by preferential activation of cGMP-primed PKG

Karnam S. Murthy

Departments of Physiology and Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0711

The singular effects and interplay of cAMP- and cGMP-dependent protein kinase (PKA and PKG) on Ca2+ mobilization were examined in dispersed smooth muscle cells. In permeabilized muscle cells, exogenous cAMP and cGMP inhibited inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release and muscle contraction via PKA and PKG, respectively. A combination of cAMP and cGMP caused synergistic inhibition that was exclusively mediated by PKG and attenuated by PKA. In intact muscle cells, low concentrations (10 nM) of isoproterenol and sodium nitroprusside (SNP) inhibited agonist-induced, IP3-dependent Ca2+ release and muscle contraction via PKA and PKG, respectively. A combination of isoproterenol and SNP increased PKA and PKG activities: the increase in PKA activity reflected inhibition of phosphodiesterase 3 activity by cGMP, whereas the increase in PKG activity reflected activation of cGMP-primed PKG by cAMP. Inhibition of Ca2+ release and muscle contraction by the combination of isoproterenol and SNP was preferentially mediated by PKG. In light of studies showing that PKG phosphorylates the IP3 receptor in intact and permeabilized muscle cells, whereas PKA phosphorylates the receptor in permeabilized cells only, the results imply that inhibition of IP3-induced Ca2+ release is mediated exclusively by PKG. The effect of PKA on agonist-induced Ca2+ release probably reflects inhibition of IP3 formation.

smooth muscle; relaxation; protein kinase; 1,4,5-trisphosphate


This article has been cited by other articles:


Home page
 Pharmacol. Rev.Home page
R. Laporte, A. Hui, and I. Laher
Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle
Pharmacol. Rev., December 1, 2004; 56(4): 439 - 513.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
H.-L. Xu, H. M. Wolde, V. Gavrilyuk, V. L. Baughman, and D. A. Pelligrino
cAMP modulates cGMP-mediated cerebral arteriolar relaxation in vivo
Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2501 - H2509.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
X.-Z. Shi and S. K. Sarna
G protein-mediated dysfunction of excitation-contraction coupling in ileal inflammation
Am J Physiol Gastrointest Liver Physiol, June 1, 2004; 286(6): G899 - G905.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. S. Murthy and H. Zhou
Selective phosphorylation of the IP3R-I in vivo by cGMP-dependent protein kinase in smooth muscle
Am J Physiol Gastrointest Liver Physiol, February 1, 2003; 284(2): G221 - G230.
[Abstract] [Full Text] [PDF]


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