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Background <p>Hypertension remains a leading cause of cardiovascular morbidity and mortality worldwide, yet the mechanisms linking vascular dysfunction, renal sodium handling and neurohumoral dysregulation remain incompletely understood. Transient receptor potential (TRP) channels have emerged as important regulators of these processes through their effects on intracellular Ca²⁺ signalling and cellular homeostasis.</p> Objective <p>To systematically evaluate recent evidence regarding the involvement of TRP channels in hypertension, with emphasis on mechanistic pathways, physiological relevance and translational implications.</p> Methods <p>A PRISMA-guided systematic search of Web of Science, Scopus and Ovid Medline was conducted to identify studies published between 2015 and 2025 investigating TRP channel expression, activity or modulation in hypertension. Eligible studies included preclinical animal studies and human observational or mechanistic investigations. Data on blood pressure regulation, vascular function, renal sodium handling and related mechanistic outcomes were extracted. Risk of bias and certainty of evidence were assessed using established evaluation frameworks.</p> Results <p>Fifteen studies met the inclusion criteria, comprising 13 preclinical and 2 human studies. Evidence implicated multiple TRP subtypes in pathways relevant to hypertension, including endothelial dysfunction, vascular smooth muscle regulation, renal sodium handling, immune–mitochondrial interactions and sympathetic activation. Although the effects of individual channels varied according to cellular localisation, vascular bed and disease context, disturbances in Ca²⁺ signalling emerged as a recurring mechanistic feature linking TRP channel activity to vascular dysfunction, oxidative stress and blood pressure dysregulation. Human evidence remained limited and was largely restricted to altered TRPC3 and TRPC6 expression or activity in hypertensive individuals.</p> Conclusions <p>Current evidence supports the biological plausibility of TRP channel involvement in hypertension and highlights their participation in several interconnected mechanisms governing blood pressure regulation. However, the available evidence remains predominantly preclinical, and substantial heterogeneity exists across experimental models, vascular territories and channel subtypes. Further human studies are required to clarify the clinical relevance, context-specific roles and therapeutic potential of TRP-targeted interventions.</p>

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Systematic Review of Transient Receptor Potential (TRP) Channels in Hypertension: Mechanistic Evidence and Therapeutic Potential

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Shobana Kumar,
  • Shoaib Kakar,
  • Arutchelvan Rajamanikam,
  • Kayatri Govindaraju

摘要

Background

Hypertension remains a leading cause of cardiovascular morbidity and mortality worldwide, yet the mechanisms linking vascular dysfunction, renal sodium handling and neurohumoral dysregulation remain incompletely understood. Transient receptor potential (TRP) channels have emerged as important regulators of these processes through their effects on intracellular Ca²⁺ signalling and cellular homeostasis.

Objective

To systematically evaluate recent evidence regarding the involvement of TRP channels in hypertension, with emphasis on mechanistic pathways, physiological relevance and translational implications.

Methods

A PRISMA-guided systematic search of Web of Science, Scopus and Ovid Medline was conducted to identify studies published between 2015 and 2025 investigating TRP channel expression, activity or modulation in hypertension. Eligible studies included preclinical animal studies and human observational or mechanistic investigations. Data on blood pressure regulation, vascular function, renal sodium handling and related mechanistic outcomes were extracted. Risk of bias and certainty of evidence were assessed using established evaluation frameworks.

Results

Fifteen studies met the inclusion criteria, comprising 13 preclinical and 2 human studies. Evidence implicated multiple TRP subtypes in pathways relevant to hypertension, including endothelial dysfunction, vascular smooth muscle regulation, renal sodium handling, immune–mitochondrial interactions and sympathetic activation. Although the effects of individual channels varied according to cellular localisation, vascular bed and disease context, disturbances in Ca²⁺ signalling emerged as a recurring mechanistic feature linking TRP channel activity to vascular dysfunction, oxidative stress and blood pressure dysregulation. Human evidence remained limited and was largely restricted to altered TRPC3 and TRPC6 expression or activity in hypertensive individuals.

Conclusions

Current evidence supports the biological plausibility of TRP channel involvement in hypertension and highlights their participation in several interconnected mechanisms governing blood pressure regulation. However, the available evidence remains predominantly preclinical, and substantial heterogeneity exists across experimental models, vascular territories and channel subtypes. Further human studies are required to clarify the clinical relevance, context-specific roles and therapeutic potential of TRP-targeted interventions.