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Titlebook: Endothelin and Its Inhibitors; Timothy D. Warner Book 2001 Springer-Verlag Berlin Heidelberg 2001 Circulation.Endothelin.Glatte Muskulatur

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11#
發(fā)表于 2025-3-23 19:11:14 | 只看該作者
Jana Maeffert,Christiane Tennhardtroduced embryonic anomalies, few people anticipated a developmental role for ET-1, which was commonly regarded as a potent vasoconstrictor and pressor peptide mainly produced by vascular endothelial cells (Masaki 1995; Levin 1995). At that time only a few signaling molecules had been demonstrated id
12#
發(fā)表于 2025-3-24 00:54:58 | 只看該作者
13#
發(fā)表于 2025-3-24 03:57:49 | 只看該作者
Koichi Kato,Eva L. Feldman,Jiro Nakamurauce intense vasoconstriction of the underlying smooth muscle and so maintain endogenous vascular tone. ET-l released from other epithelial cells situated at the interface between biological compartments may have a range of actions in humans as well as functioning as a neuropeptide in the brain. Over
14#
發(fā)表于 2025-3-24 07:36:40 | 只看該作者
15#
發(fā)表于 2025-3-24 13:28:26 | 只看該作者
16#
發(fā)表于 2025-3-24 16:30:19 | 只看該作者
,Crowdfunding in der Europ?ischen Union,nglasting hypertensive response when administered intravenously in most animal species (Table 1). The characteristic biphasic response to endothelin-1 was early on explained by Warner et al. (1989). That group suggested that the biphasic response to the peptide may be due to concomitant activation o
17#
發(fā)表于 2025-3-24 20:46:36 | 只看該作者
General Framework of Preconditionerssidues (Yanagisawa et al. 1988). Three distinct members of the ET family, namely ET-1, ET-2, and ET-3, have been identified in humans through cloning (Inoue et al. 1989). The effects of ETs on mammalian organs and cells are initiated by their binding to high affinity G-protein linked receptors (see
18#
發(fā)表于 2025-3-25 02:36:40 | 只看該作者
19#
發(fā)表于 2025-3-25 05:08:53 | 只看該作者
20#
發(fā)表于 2025-3-25 09:53:36 | 只看該作者
https://doi.org/10.1007/978-3-322-97136-4ficient gas exchange. One critical aspect of pulmonary vascular physiology is the ability of the lung circulation to adapt to large variations in cardiac output with minimal impedance to blood flow at all levels (Voelkel and Weir 2000). In patients with PH, this ability is compromised, usually becau
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