The role of subtypes of voltage-gated K+ channels in pulmonary vasoconstriction induced by 15-hydroeicosatetraenoic acid.
- Author:
Qian LI
1
;
Rong ZHANG
;
Chang-Lian LÜ
;
Yan LIU
;
Zhen WANG
;
Da-Ling ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Hypoxia; Cells, Cultured; Hydroxyeicosatetraenoic Acids; pharmacology; Hypoxia; physiopathology; Kv1.5 Potassium Channel; biosynthesis; genetics; Male; Muscle, Smooth, Vascular; cytology; Myocytes, Smooth Muscle; cytology; metabolism; Potassium Channels, Voltage-Gated; antagonists & inhibitors; Pulmonary Artery; physiopathology; RNA, Messenger; biosynthesis; genetics; Rats; Rats, Wistar; Shab Potassium Channels; biosynthesis; genetics; Vasoconstriction; drug effects
- From: Acta Pharmaceutica Sinica 2006;41(5):412-417
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo observe the effect of subtypes of Kv channels in rat pulmonary artery smooth muscle cells (PASMCs) on the process of pulmonary vasoconstriction induced by 15-HETE.
METHODSIn the present study, ring of rabbit PA with specific Kv channel blockers were employed to functionally identify certain channel subtypes that took part in the process of 15-HETE induced pulmonary vasoconstriction; RT-PCR and Western blotting analysis were also used to measure the expression of subtypes of Kv in PASMCs exposed to 15-HETE,chronic hypoxia.
RESULTSBlocking of Kv1. 1, Kv1. 2, Kv1. 3 and Kv1. 6 channels did not affect 15-HETE induced vasoconstriction in normoxic rats; 15-HETE did not affect expression of Kv1. 1 and Kv1. 2 channels; 15-HETE significantly downregulated the expression of mRNA and protein of Kv1. 5 and Kv2. 1 in rat PASMCs.
CONCLUSIONThe results suggested that hypoxia may block Kv1. 5 and Kv2. 1 channels via 15-HETE mediated mechanism, leading to decrease numbers of functional Kv1. 5 and Kv2. 1 channels in PASMCs, leading to PA vasoconstriction.
