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Cardiovascular Research 2002 53(1):97-104; doi:10.1016/S0008-6363(01)00422-9
© 2002 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Reduction of Ca2+ channel activity by hypoxia in human and porcine coronary myocytes

T Smania, A Hernándezb, J Ureñaa, A.G Castellanoa, A Franco-Obregóna, A Ordoñezb and J López-Barneoa,*

aLaboratorio de Investigaciones Biomédicas, Edificio de Laboratorios, 2 planta, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Avenida Manuel Siurot s/n, E-41013 Seville, Spain
bUnidad de Cirugía Cardiovascular, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Avenida Manuel Siurot s/n, E-41013 Seville, Spain

* Corresponding author. Tel.: +34-954-617090 or +34-955-012648; fax: +34-954-617301 lbarneo{at}hvr.sas.cica.es

Objective: Oxygen (O2) tension is a major regulator of blood flow in the coronary circulation. Hypoxia can produce vasodilation through activation of ATP regulated K+ (KATP) channels in the myocyte membrane, which leads to hyperpolarization and closure of voltage-gated Ca2+ channels. However, there are other O2-sensitive mechanisms intrinsic to the vascular smooth muscle since hypoxia can relax vessels precontracted with high extracellular K+, a condition that prevents hyperpolarization following opening of K+ channels. The objective of the present study was to determine whether inhibition of Ca2+ influx through voltage-dependent channels participates in the response of coronary myocytes to hypoxia. Methods: Experiments were performed on porcine anterior descendent coronary arterial rings and on enzymatically dispersed human and porcine myocytes of the same artery. Cytosolic [Ca2+] was measured by microfluorimetry and whole-cell currents were recorded with the patch clamp technique. Results: Hypoxia (O2 tension{approx}20 mmHg) dilated endothelium-denuded porcine coronary arterial rings precontracted with high K+ in the presence of glibenclamide (5 µM), a blocker of KATP channels. In dispersed human and porcine myocytes, low O2 tension decreased basal cytosolic [Ca2+] and transmembrane Ca2+ influx independently of K+ channel activation. In patch clamped cells, hypoxia reversibly inhibited L-type Ca2+ channels. RT–PCR indicated that rHT is the predominant mRNA variant of the {alpha}1C Ca2+ channel subunit in human coronary myocytes. Conclusion: Our study demonstrates, for the first time in a human preparation, that voltage-gated Ca2+channels in coronary myocytes are under control of O2 tension.

KEYWORDS Ca-channel; Calcium (cellular); Coronary circulation; Hypoxia/anoxia; Myocytes


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