Modulation of vasomotor tone by hypoxia in the pulmonary circulation. (360G-Wellcome-078075_Z_05_Z)

£498,929

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive mechanism which diverts blood from areas of alveolar hypoxia, thereby optimising ventilation-perfusion matching. However, with global hypoxia, (e.g. in COPD), HPV causes detrimental increases in pulmonary artery pressure, increasing morbidity and mortality. The mechanisms causing HPV are controversial. The prevailing hypothesis is that HPV is caused by K+ channel inhibition, leading to depolarisation and Ca2+ influx through voltage-gated Ca2+ channels. Recently, we have been instrumental in developing an alternative model, which proposes that HPV is due to Ca2+ influx via non-selective cation channels and an endothelium-dependent Ca2+ sensitisation. We have also presented evidence that mitochondria act as the O2 sensor, although the intermediate signalling pathways remain obscure.Our major goal for the Programme is to define the Ca2+influx, release and homeostatic pathways involved in HPV. In particular we will explore the involvement of Trp channels, membrane depolarisation, and themitochondria. Our second goal is to establish the mechanisms underlying Ca2+

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Grant Details

Amount Awarded 498929
Applicant Surname Ward
Approval Committee Physiological Sciences Funding Committee
Award Date 2005-11-07T00:00:00+00:00
Financial Year 2005/06
Grant Programme: Title Project Grant
Internal ID 078075/Z/05/Z
Lead Applicant Prof Jeremy Ward
Other Applicant(s) Dr Philip Aaronson, Dr Vladimir Snetkov
Partnership Value 498929
Planned Dates: End Date 2009-04-30T00:00:00+00:00
Planned Dates: Start Date 2006-01-01T00:00:00+00:00
Recipient Org: Country United Kingdom
Region Greater London