ArticleClinical science (London, England : 1979)2019
Pharmacological inhibition of TRPV4 channels protects against ischemia-reperfusion-induced renal insufficiency in neonatal pigs.
Article in Clinical science (London, England : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The critical role of ion channels in kidney disease: perspective from AKI and CKD.Renal failure · 2025Review
- Transient receptor potential vanilloid 4 channel inhibition attenuates lung ischemia-reperfusion injury in a porcine lung transplant model.The Journal of thoracic and cardiovascular surgery · 2024Article
- Milestone Papers on Signal Transduction Mechanisms of Hypertension and Its Complications.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Activation of renal vascular smooth muscle TRPV4 channels by 5-hydroxytryptamine impairs kidney function in neonatal pigs.Microvascular research · 2023Article
- KAmerican journal of physiology. Renal physiology · 2022Article
- Role of Transient Receptor Potential Vanilloid 4 in Vascular Function.Frontiers in molecular biosciences · 2021Review
- Renal vascular TRP channels.Current research in physiology · 2021Article
- Large animal models for translational research in acute kidney injury.Renal failure · 2020Review
- TRPV4: A Physio and Pathophysiologically Significant Ion Channel.International journal of molecular sciences · 2020Review
- Nanoparticles-Mediated Modulation of TRP Channels: Advances and Therapeutic Potential.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Renal vasoconstriction, an early manifestation of ischemic acute kidney injury (AKI), results in renal hypoperfusion and a rapid decline in kidney function. The pathophysiological mechanisms that underlie ischemia-reperfusion (IR)-induced renal insufficiency are poorly understood, but possibilities include alterations in ion channel-dependent renal vasoregulation. In the present study, we show that pharmacological activation of TRPV4 channels constricted preglomerular microvessels and elicited renal hypoperfusion in neonatal pigs. Bilateral renal ischemia followed by short-term reperfusion increased TRPV4 protein expression in resistance size renal vessels and TRPV4-dependent cation currents in renal vascular smooth muscle cells (SMCs). Selective TRPV4 channel blockers attenuated IR-induced reduction in total renal blood flow (RBF), cortical perfusion, and glomerular filtration rate (GFR). TRPV4 inhibition also diminished renal IR-induced increase in AKI biomarkers. Furthermore, the level of angiotensin II (Ang II) was higher in the urine of IR- compared with sham-operated neonatal pigs. IR did not alter renal vascular expression of Ang II type 1 (AT
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