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. 2021 Sep 12;116(1):51. doi: 10.1007/s00395-021-00891-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Nitric oxide in pulmonary and systemic vasomotor control in DM + HC + CKD and Healthy swine. Transpulmonary gradient (TPG) as a function of cardiac index markedly increased as a result of endothelial nitric oxide synthase inhibition (NOSi) in both Healthy (A) and DM + HC + CKD (D) both at rest and during exercise. NOSi resulted in a similar increase in pulmonary vasoconstriction, as evidenced by the increase in pulmonary vascular resistance (PVR), in Healthy (B) and DM + HC + CKD swine (E). Nitric oxide synthase inhibition (NOSi) has a more pronounced effect on systemic vascular resistance (SVR) in DM + HC + CKD (F) than in Healthy swine (C). Healthy n = 7, DM + HC + CKD n = 7 at rest and n = 5 during exercise. Values are mean ± SEM. *P ≤ 0.05 for effect NOSi within group, ^†P ≤ 0.05 for interaction NOSi × cardiac index (D) or NOSi × BVO₂ (E) within group. ^‡P ≤ 0.05 for interaction NOSi × group (F)