hc-067047 has been researched along with Hyperemia* in 2 studies
2 other study(ies) available for hc-067047 and Hyperemia
| Article | Year |
|---|---|
TRPV4 channel blockade does not modulate skin vasodilation and sweating during hyperthermia or cutaneous postocclusive reactive and thermal hyperemia.
Transient receptor potential vanilloid 4 (TRPV4) channels exist on vascular endothelial cells and eccrine sweat gland secretory cells in human skin. Here, we assessed whether TRPV4 channels contribute to cutaneous vasodilation and sweating during whole body passive heat stress ( Topics: Adult; Female; Humans; Hyperemia; Hyperthermia; Leucine; Male; Membrane Transport Modulators; Microdialysis; Morpholines; Piperidines; Pyrroles; Quinolines; Regional Blood Flow; Skin; Sulfonamides; Sweating; Time Factors; TRPV Cation Channels; Vasodilation; Young Adult | 2021 |
Activation of TRPV4 channels does not mediate inversion of neurovascular coupling after SAH.
Neurovascular coupling (NVC) allows increased blood flow to metabolically active neurons and involves the Ca²⁺ -dependent release of vasodilator influences by astrocyte endfeet that encase parenchymal arterioles. We previously reported inversion of NVC from dilation to constriction in brain slices from subarachnoid hemorrhage (SAH) model rats. Corresponding to NVC inversion, there was a marked increase in the amplitude of spontaneous Ca²⁺ oscillations in astrocyte endfeet. Calcium-permeable transient receptor potential vanilloid (TRPV)-4 channels have been reported in astrocyte endfeet, and activators of these channels enhance Ca²⁺ oscillations in healthy animals. Here, we examined the role of TRPV4 channels in the development of high-amplitude spontaneous Ca²⁺ oscillations in astrocyte endfeet and the inversion of neurovascular coupling after SAH. Treatment of brain slices with the TRPV4 channel antagonist, HC-067047 (10 μM), did not alter the amplitude of spontaneous Ca²⁺ oscillations after SAH. In addition, HC-067047 did not inhibit or change SAH-induced inversion of neurovascular coupling. In summary, TRPV4 channels do not appear to be involved in the inversion of neurovascular coupling after SAH. Further studies examining the impact of SAH on additional Ca²⁺ signaling pathways in astrocytes are likely to reveal valuable insights into new therapeutic strategies to advance SAH treatments. Topics: Animals; Astrocytes; Calcium Signaling; Disease Models, Animal; Hyperemia; Male; Morpholines; Organ Culture Techniques; Pyrroles; Rats, Sprague-Dawley; Subarachnoid Hemorrhage; TRPV Cation Channels | 2015 |