Role of calcium channels responsible for phenylephrine-induced contraction in rat aorta 3 days after acute myocardial infarction.
10.4097/kjae.2014.66.2.143
- Author:
Jung Eun KIM
1
;
Byung Ki CHOI
;
Jun Young CHOI
;
Taeha RYU
;
Woon Seok ROH
;
Seok Young SONG
Author Information
1. Department of Anesthesiology and Pain Medicine, School of Medicine, Catholic University of Daegu, Daegu, Korea. anessy73@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Calcium channels;
Calcium influx;
Myocardial infarction;
Phenylephrine
- MeSH:
Animals;
Aorta*;
Calcium Channels*;
Calcium*;
Calcium-Transporting ATPases;
Glycerol;
Lipase;
Myocardial Infarction*;
Nifedipine;
Phenylephrine;
Rats*;
Sodium-Calcium Exchanger;
Thapsigargin
- From:Korean Journal of Anesthesiology
2014;66(2):143-152
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Phenylephrine (PE) produces tonic contraction through involvement of various calcium channels such as store-operated calcium channels (SOCCs) and voltage-operated calcium channels (VOCCs). However, the relative contribution of each calcium channel to PE-induced contraction has not been investigated in isolated rat aorta of early acute myocardial infarction (AMI). METHODS: Endothelium-denuded rat aortic rings from rats 3 days after AMI or sham-operated (SHAM) rats were prepared in an organ chamber with Krebs-Ringer bicarbonate solution for isometric tension recording. We assessed the PE dose-response relationships in 2.5 mM calcium medium for both groups. The same procedure was repeated using rings pretreated with the SOCC inhibitor 2-aminoethoxydiphenyl borate, sarco/endoplasmic-reticulum calcium ATPase inhibitor thapsigargin (TG), diacyl glycerol lipase inhibitor RHC80267, and sodium-calcium exchanger inhibitor 3,4-dichlorobenzamil hydrochloride for 30 minutes before addition of calcium. When ongoing tonic contraction was sustained, dose-response curves to the VOCC inhibitor nifedipine were obtained to assess the relative contribution of each calcium channel under various conditions. RESULTS: The effect of SOCC induction with TG pretreatment on PE-induced contraction was significantly lower in the AMI group compared to the SHAM group. In addition, there were significant decreases in the sensitivity and efficacy of the VOCC inhibitor nifedipine on PE-induced contraction in the AMI group. CONCLUSIONS: Results suggest that the change of vascular reactivity of PE in rat aorta 3 days after AMI is characterized by a decreased contribution of L-type VOCCs. The enhanced VOCC-independent calcium entry mechanisms after AMI can be mediated by enhanced capacitative calcium entry through the activation of SOCCs.
