期刊
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
卷 57, 期 2, 页码 154-165出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e3182016adf
关键词
K+ channels; STOCs; freshly isolated cells; long-term effects
资金
- Leenaards Foundation
- Emma Muschamp Foundation
- Fern Moffat Foundation
- Eagle Foundation
- Societe Academique Vaudoise
- Department of Pediatrics of the University Hospital of Lausanne
Exposure to perinatal hypoxia results in alteration of the adult pulmonary circulation, which is linked among others to alterations in K+ channels in pulmonary artery (PA) smooth muscle cells. In particular, large conductance Ca2+-activated K+ (BKCa) channels protein expression and activity were increased in adult PA from mice born in hypoxia compared with controls. We evaluated long-term effects of perinatal hypoxia on the cyclic adenosine monophosphate (cAMP)/-protein kinase A (PKA) pathway-mediated activation of BKCa channels, using isoproterenol, forskolin, and dibutyryl-cAMP. Whole-cell outward current was higher in pulmonary artery smooth muscle cells from mice born in hypoxia compared with controls. Spontaneous transient outward currents, representative of BKCa activity, were present in a greater proportion in pulmonary artery smooth muscle cells of mice born in hypoxia than in controls. Agonists induced a greater relaxation in PA of mice born in hypoxia compared with controls, and BKCa channels contributed more to the cAMP/PKA-mediated relaxation in case of perinatal hypoxia. In summary, perinatal hypoxia enhanced cAMP-mediated BKCa channels activation in adult murine PA, suggesting that this pathway could be a potential target for modulating adult pulmonary vascular tone after perinatal hypoxia.
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