Key result
Src family tyrosine kinases and potassium channels such as KV1.5 play important roles in the unique structural and functional properties of the pulmonary vascular bed.
This paper reviews the molecular mechanisms, including the role of Src family tyrosine kinases and potassium channels, underlying hypoxia-induced vasoconstriction in the pulmonary vascular bed.
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Unique pulmonary vascular properties warrant consideration in PH assessment; leaves open targeted interventions in hypoxia.
The pulmonary blood vessels have unique structural and functional properties. The pulmonary circulation is a high-flow, low-resistance, low-pressure system, which is mainly explained by two important characteristics of the pulmonary vascular bed: a high compliance of the pulmonary pre-capillary arterioles characterised by thin media and a high capacity to recruit vessels available to cope with an increase in blood flow. Local variations in response to various vasoactive molecules, such as hypoxia and nitric oxide, are well known, but the molecular mechanisms underlying the sensing of those stimuli remain obscure. In contrast to the systemic arteries, the hypoxic stimulus induces vasoconstriction of the pulmonary arteries, an effect that is more pronounced as the vessel diameter decreases [1, 2]. Different potassium channels are expressed and distributed in several types of pulmonary arterial smooth muscle cells (PA-SMCs) and contribute to this large functional diversity. Although voltage-gated potassium channel (KV)1.2, KV1.5, KV2.1, KV3.1b and KV9.3 play important roles in the hypoxia-inhibited potassium current found in PA-SMCs, much attention has been attracted by KV1.5 [3]. …
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Guignabert et al. (2012) reported a review. Src family tyrosine kinases was evaluated. Src family tyrosine kinases and potassium channels such as KV1.5 play important roles in the unique structural and functional properties of the pulmonary vascular bed.
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