Publication date: Available online 20 February 2017
Source:The Journal of Steroid Biochemistry and Molecular Biology
Author(s): Katesirin Ruamyod, Wattana B. Watanapa, Chairat Shayakul
Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.03–3μM testosterone significantly induced a rapid, concentration-dependent increase in total HCAEC current (EC50, 71.96±1.66nM; maximum increase, 59.13±8.37%; mean±SEM). The testosterone-enhanced currents consisted of small- and large-conductance Ca2+-activated K+ currents (SKCa and BKCa currents), but not Cl− and nonselective cation currents. Either a non-permeant testosterone conjugate or the non-aromatizable androgen dihydrotestosterone (DHT) could increase HCAEC currents as well. The androgen receptor antagonist flutamide prevented this testosterone, testosterone conjugate, and DHT effect, while the estrogen receptor antagonist fulvestrant did not. Incubating HCAECs with pertussis toxin or protein kinase A inhibitor H-89 largely inhibited the testosterone effect, while pre-incubation with phospholipase C inhibitor U-73122, prostacyclin inhibitor indomethacin, nitric oxide synthase inhibitor L-NAME or cytochrome P450 inhibitor MS-PPOH, did not. Finally, testosterone application induced HCAEC hyperpolarization within minutes; this effect was prevented by SKCa and BKCa current inhibitors apamin and iberiotoxin. This is the first electrophysiological demonstration of androgen-induced KCa current increase, leading to hyperpolarization, in any endothelial cell, and the first report of SKCa as a testosterone target. Our data show that testosterone rapidly increased whole-cell HCAEC SKCa and BKCa currents via a surface androgen receptor, Gi/o protein, and protein kinase A. This mechanism may explain rapid testosterone-induced coronary vasodilation seen in vivo.
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Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com
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Τρίτη 21 Φεβρουαρίου 2017
Testosterone rapidly increases Ca2+-activated K+ currents causing hyperpolarization in human coronary artery endothelial cells
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- Pepsin as a biomarker for laryngopharyngeal reflux...
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- The current status of human laryngeal transplantat...
- Customized software to optimize circumferential ph...
- Clinical effect of intratympanic dexamethasone inj...
- Laboratory assessment of sudden sensorineural hear...
- Customized software to optimize circumferential ph...
- Quality of life of patients who underwent aestheti...
- Laboratory assessment of sudden sensorineural hear...
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- Quality of life of patients who underwent aestheti...
- The repeatability of tests of eustachian tube func...
- Compound motor action potential duration and laten...
- Impacts of disease severity on postoperative compl...
- The repeatability of tests of eustachian tube func...
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- Impacts of disease severity on postoperative compl...
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- Intranasal trigeminal function in patients with em...
- Can contaminated water be rendered safe for nasal ...
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