Neurovascular coupling protects neurons against hypoxic injury via inhibition of potassium currents by generation of nitric oxide in direct neuron and endothelium cocultures

Neuroscience ◽  
2016 ◽  
Vol 334 ◽  
pp. 275-282 ◽  
Author(s):  
Kun-Wei Wu ◽  
Zeng-Wei Kou ◽  
Jia-Lin Mo ◽  
Xu-Xu Deng ◽  
Feng-Yan Sun
Keyword(s):  
Nitric Oxide ◽  
Neurovascular Coupling ◽  
Potassium Currents ◽  
Hypoxic Injury

scholarly journals Attenuated outward potassium currents in carotid body glomus cells of heart failure rabbit: involvement of nitric oxide

2004 ◽  
Vol 555 (1) ◽  
pp. 219-229 ◽  
Author(s):  
Yu-Long Li ◽  
Shu-Yu Sun ◽  
Jeffery L. Overholt ◽  
Nanduri R. Prabhakar ◽  
George J. Rozanski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Carotid Body ◽  
Potassium Currents ◽  
Glomus Cells ◽  
Carotid Body Glomus Cells

scholarly journals Nitric oxide, KATP channels and endothelin-1 modulate brain pericyte function, vascular tone and neurovascular coupling

2020 ◽  
Author(s):  
Stefan Andreas Zambach ◽  
Changsi Cai ◽  
Hans Christian Cederberg Helms ◽  
Bjørn Olav Hald ◽  
Jonas Christoffer Fordsmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vascular Tone ◽  
Functional Neuroimaging ◽  
Neurovascular Coupling ◽  
Katp Channels ◽  
Capillary Blood ◽  
Local Synthesis ◽  
Endothelin 1 ◽  
Brain Pericytes

ABSTRACTNeurotransmitter-mediated signaling correlates strongly to changes in cerebral blood flow (CBF), and functional neuroimaging relies on the robust coupling between activity and CBF, i.e. neurovascular coupling (NVC). We here reveal that key endothelial signaling molecules, nitric oxide (eNO) and endothelin-1 (ET1), modulate pericyte contractility and that pericyte ATP-sensitive potassium (KATP) channels interact with endothelial factors to modulate vascular tone and NVC. We show that NVC requires local synthesis of cGMP, but not NO derived from endothelial cells. The potent endothelial vasoconstrictor ET1 contracted pericytes by IP3 receptor mediated Ca2+ release and blocked NVC. In comparison, pericyte KATP channel openers increased the diameter of capillaries by deactivation of L-type Ca2+ channels while KATP blockers shortened the NVC response. All vasoactive stimuli produced the largest diameter changes at the first capillary that branches off from the penetrating arteriole. Our results reveal that three different signaling pathways mediate the effects of NO, ET1 and KATP channels on brain pericytes and capillary blood flow by mechanisms similar to vascular smooth muscle despite great differences in morphology.

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