TRPV4‐mediated responses of the rat isolated cremaster muscle artery
Autor: | Arjna Kanagarajah, Timothy V. Murphy, Sevvandi Senadheera, Shaun L. Sandow |
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Rok vydání: | 2013 |
Předmět: | |
Zdroj: | The FASEB Journal. 27 |
ISSN: | 1530-6860 0892-6638 |
DOI: | 10.1096/fasebj.27.1_supplement.901.10 |
Popis: | Transient receptor potential (TRP) channels are a family of ion channels with emerging roles in the vasculature. This study investigated the expression and function of TRPV4 channels in isolated, pressurized (70 mmHg) rat cremaster muscle arteries with myogenic tone. Immunohistochemistry showed TRPV4 was present at a low level in the endothelium and smooth muscle of the arteries. The TRPV4 activator RN1747 caused a concentration-dependent dilation of the arteries (EC50 18.0 ± 0.2 μM, n = 14). The TRPV4 inhibitor RN1734 (10 and 30 μM) caused a modest rightward-shift of the RN1747 concentration-response curve. The Ca2+-activated K+ channel (KCa) inhibitor TEA (1 mM) also inhibited responses to RN1747 and the effects of RN1734 and TEA were additive. RN1734 did not inhibit endothelium-dependent vasodilation of the arteries induced by acetylcholine, but endothelium-independent vasodilation caused by adenosine was inhibited by RN1734. TEA also inhibited responses to adenosine and the effects of RN1734 and TEA were additive. In conclusion, TRPV4 was present in the endothelium and smooth muscle of cremaster muscle arteries. Endothelium-dependent acetylcholine-mediated vasodilation did not occur via TRPV4 channels, but adenosine-mediated vasodilation occurred via TRPV4. The role of KCa channels in TRPV4 responses remains to be clarified. RN1747 may be an agent of limited use in in vitro studies of the vasculature. |
Databáze: | OpenAIRE |
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