Restoration of Vitamin D Levels Improves Endothelial Function and Increases TASK-Like K+ Currents in Pulmonary Arterial Hypertension Associated with Vitamin D Deficiency
| Autor: | Francisco Perez-Vizcaino, Bianca Barreira, Daniel Morales-Cano, Laura Moreno, Miguel A Olivencia, Angel Cogolludo, María Callejo, Sergio Esquivel-Ruiz, Gema Mondejar-Parreño |
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| Rok vydání: | 2021 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Hemodynamics Dietética y nutrición Nerve Tissue Proteins Vasodilation 030204 cardiovascular system & hematology Cardiología Biochemistry Microbiology Article vitamin D deficiency Membrane Potentials Muscle hypertrophy vascular function Contractility 03 medical and health sciences Potassium Channels Tandem Pore Domain 0302 clinical medicine Internal medicine pulmonary hypertension medicine Vitamin D and neurology Animals vitamin D supplementation Rats Wistar Vitamin D Endothelial dysfunction Molecular Biology Neumología Pulmonary Arterial Hypertension business.industry Vitamin D Deficiency medicine.disease Pulmonary hypertension QR1-502 Rats 030104 developmental biology Endocrinology Endothelium Vascular business TASK-1 channel |
| Zdroj: | E-Prints Complutense. Archivo Institucional de la UCM instname Biomolecules Volume 11 Issue 6 Biomolecules, Vol 11, Iss 795, p 795 (2021) |
| Popis: | Background: Vitamin D (vitD) deficiency is highly prevalent in patients with pulmonary arterial hypertension (PAH). Moreover, PAH-patients with lower levels of vitD have worse prognosis. We hypothesize that recovering optimal levels of vitD in an animal model of PAH previously depleted of vitD improves the hemodynamics, the endothelial dysfunction and the ionic remodeling. Methods: Male Wistar rats were fed a vitD-free diet for five weeks and then received a single dose of Su5416 (20 mg/Kg) and were exposed to vitD-free diet and chronic hypoxia (10% O2) for three weeks to induce PAH. Following this, vitD deficient rats with PAH were housed in room air and randomly divided into two groups: (a) continued on vitD-free diet or (b) received an oral dose of 100,000 IU/Kg of vitD plus standard diet for three weeks. Hemodynamics, pulmonary vascular remodeling, pulmonary arterial contractility, and K+ currents were analyzed. Results: Recovering optimal levels of vitD improved endothelial function, measured by an increase in the endothelium-dependent vasodilator response to acetylcholine. It also increased the activity of TASK-1 potassium channels. However, vitD supplementation did not reduce pulmonary pressure and did not ameliorate pulmonary vascular remodeling and right ventricle hypertrophy. Conclusions: Altogether, these data suggest that in animals with PAH and severe deficit of vitD, restoring vitD levels to an optimal range partially improves some pathophysiological features of PAH. |
| Databáze: | OpenAIRE |
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