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# Hypertension, endothelial tyrosine hydroxylase, and hypoxia
Endothelium expresses tyrosine hydroxylase (TH), and tyrosine hydroxylase gene expression increases with hypoxia (Sorriento, 2012). This is likely part of endocrine regulation of the heart by organs such as skeletal muscle.
High blood pressure compresses the vasa vasorum, and causes hypoxia in the vessel wall (Sacks, 1975).
Chronic high blood pressure leads to chronic hypoxia in the vessel wall, and necrosis.
Cholesterol is always present during wound healing. Correlates with macrophage presence (Bagnati, 2019).
A hypothetical disturbed feedback loop during chronic hypertension, hypoxia in vessel walls from compression upregulates TH, increases adrenaline synthesis and excretion from endothelium, increases cardiac output and contracts vascular system, increases blood pressure, increases compression-damage, upregulates TH, and so on.
# References
Sorriento, D., Santulli, G., Del Giudice, C., Anastasio, A., Trimarco, B., & Iaccarino, G. (2012). Endothelial Cells Are Able to Synthesize and Release Catecholamines Both In Vitro and In Vivo. Hypertension, 60(1), 129 136. https://doi.org/10.1161/hypertensionaha.111.189605
Sacks, A. H. (1975). The Vasa Vasorum as a Link Between Hypertension and Arteriosclerosis. Angiology, 26(5), 385 390. https://doi.org/10.1177/000331977502600503
Bagnati, M., Moreno-Moral, A., Ko, J.-H., Nicod, J., Harmston, N., Imprialou, M., Game, L., Gil, J., Petretto, E., & Behmoaras, J. (2019). Systems genetics identifies a macrophage cholesterol network associated with physiological wound healing. JCI Insight, 4(2). https://doi.org/10.1172/jci.insight.125736