| Regulation of L-type inward calcium channel activity by captopril and angiotensin II via the phosphatidyl inositol 3-kinase pathway in cardiomyocytes from volume-overload hypertrophied rat hearts. | |
| | |
MedLine Citation:
|
PMID: 21423294 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Heart failure can be caused by pro-hypertrophic humoral factors such as angiotensin II (Ang II), which regulates protein kinase activities. The intermingled responses of these kinases lead to the early compensated cardiac hypertrophy, but later to the uncompensated phase of heart failure. We have shown that although beneficial, cardiac hypertrophy is associated with modifications in ion channels that are mainly mediated through mitogen-activated protein (MAP) kinase and phosphatidylinositol 3-kinase (PI3K) activation. This study evaluates the control of L-type Ca(2+) current (I(Ca,L)) by the Ang II/PI3K pathway in hypertrophied ventricular myocytes from volume-overload rats using the perforated patch-clamp technique. To assess activation of the I(Ca,L) in cardiomyocytes, voltages of 350 ms in 10 mV increments from a holding potential of -85 mV were applied to cardiocytes, with a pre-pulse to -45 mV for 300 ms. Volume overload-induced hypertrophy reduces I(Ca,L), whereas addition of Ang II alleviates the hypertrophic-induced decrease in a PI3K-dependent manner. Acute administration of Ang II (10(-6) mol/L) to normal adult cardiomyocytes had no effect; however, captopril reduced their basal I(Ca,L). In parallel, captopril regressed the hypertrophy and inverted the Ang II effect on I(Ca,L) seemingly through a PI3K upstream effector. Thus, it seems that regression of cardiac hypertrophy by captopril improved I(Ca,L) partly through PI3K. |
| | |
Authors:
|
Zikiar Alvin; Graham G Laurence; Bernell R Coleman; Aiqiu Zhao; Majd Hajj-Moussa; Georges E Haddad |
Related Documents
:
|
8378304 - Persistent activation of the zeta isoform of protein kinase c in the maintenance of lon... 1386624 - Postsynaptic, but not presynaptic, activity controls the early time course of long-term... 9704994 - Involvement of calcium/calmodulin-dependent protein kinases in the setting of a molecul... 17286594 - Serotonin and neuronal growth factors - a convergence of signaling pathways. 7479864 - Interaction between focal adhesion kinase and crk-associated tyrosine kinase substrate ... 9525964 - Binding of urokinase-type plasminogen activator to its receptor in mcf-7 cells activate... |
Publication Detail:
|
Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Canadian journal of physiology and pharmacology Volume: 89 ISSN: 1205-7541 ISO Abbreviation: Can. J. Physiol. Pharmacol. Publication Date: 2011 Mar |
Date Detail:
|
Created Date: 2011-03-22 Completed Date: 2012-02-13 Revised Date: 2012-09-20 |
Medline Journal Info:
|
Nlm Unique ID: 0372712 Medline TA: Can J Physiol Pharmacol Country: Canada |
Other Details:
|
Languages: eng Pagination: 206-15 Citation Subset: IM |
Affiliation:
|
Department of Physiology and Biophysics, College of Medicine, Howard University, WA 20059, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Angiotensin II
/
pharmacology*,
therapeutic use Animals Calcium Channels, L-Type / physiology* Captopril / pharmacology*, therapeutic use Cardiomegaly / drug therapy, enzymology* Male Myocytes, Cardiac / drug effects*, enzymology, metabolism Phosphatidylinositol 3-Kinase / antagonists & inhibitors, metabolism* Rats Rats, Sprague-Dawley Signal Transduction / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
|
2G12 RR003048/RR/NCRR NIH HHS; G12 RR003048-14/RR/NCRR NIH HHS; GM08016-38/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Calcium Channels, L-Type; 11128-99-7/Angiotensin II; 62571-86-2/Captopril; EC 2.7.1.137/Phosphatidylinositol 3-Kinase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Enalapril decreases cardiac mass and fetal gene expression without affecting the expression of endot...
Next Document: Modulation of metabolic and cardiac dysfunctions by insulin sensitizers and angiotensin receptor blo...