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|Title: ||Cellular mechanisms of acute hypoxic pulmonary vasoconstriction in intrapulmonary veins.|
|Authors: ||Dospinescu, Ciprian|
|Supervisors: ||Cruickshank, Stuart F.|
Wainwright, Cherry L.
|Keywords: ||Hypoxic pulmonary vasoconstriction|
|Issue Date: ||Mar-2009|
|Publisher: ||The Robert Gordon University|
|Citation: ||DOSPINESCU, C. and CRUICKSHANK, S. F., 2006. [cL-]o and [Ca2+]o affect hypoxia-induced contractions differently in porcine intrapulmonary arteries and veins. In: Abstracts, The Physiological Society workshop on Cardiopulmonary Function in Health and Dieease, Prague, The Czech Republic)|
DOSPINESCU, C. and CRUICKSHANK, S. F., 2006. Cl- channel blocker NFA inhibits PGF2a and hypoxia-induced contractions in porcine intrapulmonary veins but not in arteries. In: Absrracts, FASEB Summer Research Conference, Smooth Muscle, Snowmass Village, Colorado, USA.
DOSPINESCU, C., MCCAIG, D., WAINWRIGHT, C. L. and CRUICKSHANK, S. F., 2006. Different role for [Cl-]o in hypoxia induced contractions of small intrapulmonary arteries and veins. In: Journal of Molecular and Cellular Cardiology, 40 (6), pp. 1015.
DOSPINESCU, C., YAMAWAKI, N., MCCAIG, D., WAINWRIGHT, C. L. and CRUICKSHANK, S. F., 2005. Low chloride potentiation of hypoxic pulmonary vasoconstriction. In: Journal of Physiology 568P:PC44.
|Abstract: ||In the pulmonary circulation, alveolar hypoxia contributes to blood flow regulation.
Hypoxic pulmonary vasoconstriction (HPV) involves both pulmonary arteries and
veins, but little is known of the contractile mechanisms specific to the veins. The aim
of these studies was to examine the hypoxic response in small porcine
intrapulmonary veins in relation to the arterial response, and investigate the effects
of hypoxia on ion conductances in single myocytes from intrapulmonary veins.
In wire myography experiments, intrapulmonary veins contracted more than sizematched
arteries in response to hypoxia and agonists KCl and PGF2α. Venous
contractions were inhibited by removal of extracellular Ca2+ or in the presence of Clchannel
blocker NFA, effects not seen in the arteries. To examine the mechanisms of
venous contraction at cellular level, single pulmonary vein smooth muscle cells
(PVSMC) were freshly isolated and characterised morphologically and
electrophysiologically for the first time. In patch-clamp studies, hypoxia reversibly
inhibited a whole-cell outward current in the presence of BKCa channel antagonist
Penitrem A. By subtracting currents recorded in normoxia and hypoxia, a novel
hypoxia-sensitive K+ current (IK(H)) was revealed in PVSMC. IK(H) was a rapidly
activating, partially inactivating current and was sensitive to KV channel blocker
4-AP. The biophysical properties of IK(H) revealed the voltage window of current
availability with a peak near the resting membrane potential of PVSMC.
In conclusion, these findings highlight differences between the contractile properties
of veins and arteries and reveal a significant contribution of Ca2+ influx and an
NFA-sensitive conductance during venous contraction to agonists and hypoxia.
Furthermore, the results suggest that a novel hypoxia-sensitive KV current
contributes to membrane potential under resting conditions in PVSMC and its
inhibition by hypoxia may contribute to the initiation of HPV in porcine
|Appears in Collections:||Theses (Pharmacy & Life Sciences)|
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