ArticleJACC. Basic to translational science2024
Carotid Baroreceptor Stimulation Improves Pulmonary Arterial Remodeling and Right Ventricular Dysfunction in Pulmonary Arterial Hypertension.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ventricular arrhythmogenesis in pulmonary hypertension: From right ventricular remodeling to clinical implications.Physiological reports · 2026Review
- A scoping review of neuromodulation techniques for controlling blood pressure: what are the ups and downs to this approach?Bioelectronic medicine · 2025Review
- Autonomic control of the pulmonary circulation: Implications for pulmonary hypertension.Experimental physiology · 2025Review
- Comprehensive Insights into Mechanisms for Ventricular Remodeling in Right Heart Failure.Reviews in cardiovascular medicine · 2024Review
- The coming era of neuromodulation therapies: expectations for baroreceptor stimulation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Do Not Lose Your Nerves: Autonomic Neuromodulation in Pulmonary Arterial Hypertension.JACC. Basic to translational science · 2024Article
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Authors and funding
11 authors.
Funding
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Abstract
Autonomic nervous system imbalance is intricately associated with the severity and prognosis of pulmonary arterial hypertension (PAH). Carotid baroreceptor stimulation (CBS) is a nonpharmaceutical intervention for autonomic neuromodulation. The effects of CBS on monocrotaline-induced PAH were investigated in this study, and its underlying mechanisms were elucidated. The results indicated that CBS improved pulmonary hemodynamic status and alleviated right ventricular dysfunction, improving pulmonary arterial remodeling and right ventricular remodeling, thus enhancing the survival rate of monocrotaline-induced PAH rats. The beneficial effects of CBS treatment on PAH might be mediated through the inhibition of sympathetic overactivation and inflammatory immune signaling pathways.
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