# A Plant-Based Diet Alleviates Molecular Pulmonary Abnormalities in Hypertension

## TL;DR

A plant-based diet improves lung health in hypertensive rats, even without lowering overall blood pressure.

## Contribution

The study shows a plant-based diet can reverse molecular lung abnormalities in hypertension.

## Key findings

- A plant-based diet prevented and reversed reduced lung endothelial nitric oxide synthase in hypertensive rats.
- The diet improved epithelial junction proteins and reduced profibrotic signaling in the lungs.

## Abstract

What are the main findings?

A plant-based diet prevented and reversed compromised lung endothelial nitric oxide synthase in hypertensive rats, despite not impacting systemic hypertension.

A plant-based diet enhanced expression of epithelial junction proteins and atten-uated profibrotic proteins.

What are the implications of the main findings?

These positive molecular effects are associated with improved lung function and reduced lung disease in pulmonary hypertension.

A plant-based diet could be used as a treatment for pulmonary hypertension, but more research is needed.

Background: Essential hypertension is associated with an increased risk of pulmonary hypertension (PH). PH is diagnosed more frequently in females. Little is known about the effects of a plant-based diet (PBD) in improving lung abnormalities in PH. Methods: We compared 28- and 40-week-old female normotensive Wistar Kyoto and spontaneously hypertensive rats (SHR), maintained from the age of 4 weeks on a control refined diet or a PBD, comprising 28% fruits, vegetables, nuts and legumes. A subset of control SHRs were switched to the PBD at 28 weeks of age. Lungs were taken for protein and histological analysis. Results: Relative to WKYs, SHRs consuming the control diet exhibited decreased lung endothelial nitric oxide synthase (eNOS). PBD consumption by SHRs prevented and reversed this phenotype. Expression of E-cadherin was also reduced in SHRs. This reduction was attenuated by PBD consumption treatment. The phosphorylation of extracellular signal-regulated kinase (ERK)1/2 in the lung was increased in SHRs and attenuated by PBD. The expression of activated transforming growth factor (TGF)-β1 was also attenuated by a PBD. Conclusions: The PBD favorably mediated hypertension-induced pulmonary molecular abnormalities in lung endothelium, epithelial junction and pro-fibrotic signaling. Future studies should assess the effects of a PBD in improving PH and lung function.