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- W2134449012 abstract "Many pathological conditions, like sleep apnea (SA), preeclampsia, high altitude sickness, and chronic obstructive pulmonary disease, that cause intermittent or chronic hypoxia, are often associated with the development of either systemic or pulmonary hypertension.1 Mechanisms sensing hypoxia may be important contributors to the development of pulmonary hypertension and to tissue injury and repair associated with hypertensive disease and in integrated aspects of cardiovascular function. This review will focus on highlighting how some of the better documented oxygen-sensing mechanisms associated with vascular regulation could be influenced by poorly understood interactions between hypoxia and hypertension. It will also consider some of the identified integrated interactions between hypoxia and hypertensive disease processes that could contribute to the progression of disease processes, such as renal hypertension.High altitude and chronic obstructive pulmonary disease are thought to promote pulmonary hypertension by exposing the pulmonary circulation to chronic hypoxia as a result of the low partial pressure of oxygen at high altitude and increases in the diffusion distance for oxygen, respectively.2,3 Although high altitude can initially promote increased systemic blood pressure, this change appears to reverse with time.4 Interestingly, hypobaric hypoxia conditions of high altitude were observed to prevent the development of hypertension and skeletal muscle arteriolar rarefaction in spontaneously hypertensive rats.5 Living at high altitude seems to lower blood pressure only in children,6 and it did not appear to attenuate hypertension in obese adults consuming high-fat diets.7 Based on studies in animal models of acute and chronic hypoxia, hypoxic pulmonary vasoconstriction (HPV) is initially activated. Eventually endothelial dysfunction associated with a loss of NO and increased reactive oxygen species (ROS), endothelin, serotonin, and contractile prostaglandins contribute to maintaining elevated pulmonary artery pressure through increased intracellular Ca2+ levels and rho kinase-associated myofilament Ca2+ sensitivity.8 Although …" @default.
- W2134449012 created "2016-06-24" @default.
- W2134449012 creator A5033512267 @default.
- W2134449012 creator A5040548588 @default.
- W2134449012 date "2012-08-01" @default.
- W2134449012 modified "2023-09-24" @default.
- W2134449012 title "Relationships Between Vascular Oxygen Sensing Mechanisms and Hypertensive Disease Processes" @default.
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- W2134449012 doi "https://doi.org/10.1161/hypertensionaha.112.190702" @default.
- W2134449012 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3401320" @default.
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- W2134449012 hasPublicationYear "2012" @default.
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