Luminal ATP-induced contraction of rabbit pulmonary arteries and role of purinoceptors in the regulation of pulmonary arterial pressure
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- 作者：Eun Bok Baek (1)
Hae Young Yoo (1)
Su Jung Park (1)
Hyang Sun Kim (1)
Seong Deok Kim (2)
Yung E. Earm (1)
Sung Joan Kim (3) - 关键词：Adenosine 5 ; triphosphate (ATP) ; Coronary artery ; Pulmonary artery ; Hypoxic pulmonary vasoconstriction ; Purinoceptor ; P2Y purinoceptor ; P2X purinoceptor
- 刊名：Pfl眉gers Archiv - European Journal of Physiology
- 出版年：2008
- 出版时间：November 2008
- 年：2008
- 卷：457
- 期：2
- 页码：281-291
- 全文大小：304KB
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Hae Young Yoo (1)
Su Jung Park (1)
Hyang Sun Kim (1)
Seong Deok Kim (2)
Yung E. Earm (1)
Sung Joan Kim (3)
1. Department of Physiology, Seoul National University College of Medicine, Seoul, 110-799, Republic of Korea
2. Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Seoul, 110-799, Republic of Korea
3. Department of Physiology, Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, 110-799, Republic of Korea - ISSN：1432-2013
文摘
The effects of luminal ATP between rabbit pulmonary (PAs) and coronary arteries (CAs) were compared to understand the role of purinoceptors in the regulation of pulmonary arterial pressure (PAP) under hypoxia. Diameters of vessels were video analyzed under luminal perfusion. ATP-induced membrane currents and intracellular Ca2+ signals ([Ca2+]i) were compared in pulmonary (PASMCs) and coronary myocytes (CASMCs) using patch clamp and spectrofluorimetry. PAP was measured in perfused lungs under ventilation. Luminal ATP induced constriction of rabbit PAs in the presence of endothelium. In contrast, CAs showed dilating responses to luminal ATP even in the absence of endothelium. In PASMCs, both P2X-mediated inward current and P2Y-mediated store Ca2+ release were consistently observed. In contrast, CASMCs showed neither P2X nor P2Y responses. In the perfused lungs, hypoxia-induced PAP increase was decreased by suramin, a purinergic antagonist. A luminal application of α,β-meATP largely increased PAP, whereas UTP decreased PAP. The combined application of P2X- and P2Y-selective agonists (α,β-meATP and UTP) increased PAP. However, the perfusion of ATP alone decreased PAP, and the ATP-induced PAP decrease was affected neither by adenosine receptor antagonist nor by nitric oxide synthase inhibitor. In summary, although the luminal ATP constricts isolated PAs and suramin attenuated the HPV of perfused lungs, the bimodal responses of PAP to purinergic agonists indicate that the luminal ATP regulates pulmonary circulation via complex signaling interactions in situ.