Referenced in: none

Automatically associated channels: Slo1

Title: Perinatal hypoxia enhances cyclic adenosine monophosphate-mediated BKCa channel activation in adult murine pulmonary artery.

Authors: Mathieu Marino, Jean-Louis Bény, Anne-Christine Peyter, Giacomo Diaceri, Jean-François Tolsa

Journal, date & volume: J. Cardiovasc. Pharmacol., 2011 Feb , 57, 154-65

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21289495

Abstract
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 Ca(2+)-activated K(+) (BK(Ca)) 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 BK(Ca) 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 BK(Ca) 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 BK(Ca) channels contributed more to the cAMP/PKA-mediated relaxation in case of perinatal hypoxia. In summary, perinatal hypoxia enhanced cAMP-mediated BK(Ca) channels activation in adult murine PA, suggesting that this pathway could be a potential target for modulating adult pulmonary vascular tone after perinatal hypoxia.