Diabetes alters microvascular function in the vascular beds of organs including the lungs. Cardiovascular complications of pulmonary vascular affectation may be a consequence of the over-activation of the vasoconstrictive and proliferative components of the renin-angiotensin system. We previously reported that pulmonary physiology and surfactant production is improved by the GLP-1R agonist liraglutide in a rat model of lung hypoplasia. Since we hypothesized that streptozotocin-induced diabetes rats would show deficiencies in lung function including surfactant proteins and develop an imbalance of the renin-angiotensin system in the lungs.

 

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