ArticleFrontiers in pharmacology2015
The depressor response to intracerebroventricular hypotonic saline is sensitive to TRPV4 antagonist RN1734.
Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Temperature modulates PVN pre-sympathetic neurones via transient receptor potential ion channels.Frontiers in pharmacology · 2023Article
- Systemic application of the transient receptor potential vanilloid-type 4 antagonist GSK2193874 induces tail vasodilation in a mouse model of thermoregulation.Biology letters · 2022Article
- Transient receptor potential vanilloid type 4 is expressed in vasopressinergic neurons within the magnocellular subdivision of the rat paraventricular nucleus of the hypothalamus.The Journal of comparative neurology · 2018Article
- Ion Channels in the Paraventricular Hypothalamic Nucleus (PVN); Emerging Diversity and Functional Roles.Frontiers in physiology · 2018Review
- Emerging Roles of the Membrane Potential: Action Beyond the Action Potential.Frontiers in physiology · 2018Review
- Activation of transient receptor potential vanilloid 4 involves in hypoxia/reoxygenation injury in cardiomyocytes.Cell death & disease · 2017Article
- Pleiotropic function of TRPV4 ion channels in the central nervous system.Experimental physiology · 2016Review
- TRPV4 is associated with central rather than nephrogenic osmoregulation.Pflugers Archiv : European journal of physiology · 2016Article
- Small molecule dual-inhibitors of TRPV4 and TRPA1 for attenuation of inflammation and pain.Scientific reports · 2016Article
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Authors and funding
3 authors.
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Abstract
Several reports have shown that the periventricular region of the brain, including the paraventricular nucleus (PVN), is critical to sensing and responding to changes in plasma osmolality. Further studies also implicate the transient receptor potential ion channel, type V4 (TRPV4) channel in this homeostatic behavior. In previous work we have shown that TRPV4 ion channels couple to calcium-activated potassium channels in the PVN to decrease action potential firing frequency in response to hypotonicity. In the present study we investigated whether, similarly, intracerebroventricular (ICV) application of hypotonic solutions modulated cardiovascular parameters, and if so whether this was sensitive to a TRPV4 channel inhibitor. We found that ICV injection of 270 mOsmol artificial cerebrospinal fluid (ACSF) decreased mean blood pressure, but not heart rate, compared to naïve mice or mice injected with 300 mOsmol ACSF. This effect was abolished by treatment with the TRPV4 inhibitor RN1734. These data suggest that periventricular targets within the brain are capable of generating depressor action in response to TRPV4 ion channel activation. Potentially, in the future, the TRPV4 channel, or the TRPV4-KCa coupling mechanism, may serve as a therapeutic target for treatment of cardiovascular disease.
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