scholarly journals Purinergic receptor activation evokes neurotrophic factor neuropeptide Y release from neonatal mouse olfactory epithelial slices

2009 ◽  
Vol 87 (6) ◽  
pp. 1424-1434 ◽  
Author(s):  
Shami Kanekar ◽  
Cuihong Jia ◽  
Colleen Cosgrove Hegg
2021 ◽  
Vol 433 (13) ◽  
pp. 166992
Author(s):  
Miron Mikhailowitsch Gershkovich ◽  
Victoria Elisabeth Groß ◽  
Oanh Vu ◽  
Clara Tabea Schoeder ◽  
Jens Meiler ◽  
...  

2014 ◽  
Vol 34 (10) ◽  
pp. 1706-1714 ◽  
Author(s):  
Yao Li ◽  
Rachael L Baylie ◽  
Matthew J Tavares ◽  
Joseph E Brayden

Cerebral parenchymal arterioles (PAs) have a critical role in assuring appropriate blood flow and perfusion pressure within the brain. They are unique in contrast to upstream pial arteries, as defined by their critical roles in neurovascular coupling, distinct sensitivities to chemical stimulants, and enhanced myogenic tone development. The objective of the present study was to reveal some of the unique mechanisms of myogenic tone regulation in the cerebral microcirculation. Here, we report that in vivo suppression of TRPM4 (transient receptor potential) channel expression, or inhibition of TRPM4 channels with 9-phenanthrol substantially reduced myogenic tone of isolated PAs, supporting a key role of TRPM4 channels in PA myogenic tone development. Further, downregulation of TRPM4 channels inhibited vasoconstriction induced by the specific P2Y4 and P2Y6 receptor ligands (UTP γS and UDP) by 37% and 42%, respectively. In addition, 9-phenanthrol substantially attenuated purinergic ligand-induced membrane depolarization and constriction of PAs, and inhibited ligand-evoked TRPM4 channel activation in isolated PA myocytes. In concert with our previous work showing the essential contributions of P2Y4 and P2Y6 receptors to myogenic regulation of PAs, the current results point to TRPM4 channels as an important link between mechanosensitive P2Y receptor activation and myogenic constriction of cerebral PAs.


1992 ◽  
Vol 10 (10) ◽  
pp. 1303
Author(s):  
G Tavemier ◽  
C Damase-Michel ◽  
M A Tran ◽  
J L Montastruc ◽  
P Montastruc

1989 ◽  
Vol 257 (3) ◽  
pp. H866-H872 ◽  
Author(s):  
J. Pernow ◽  
J. Schwieler ◽  
T. Kahan ◽  
P. Hjemdahl ◽  
J. Oberle ◽  
...  

The effects of sympathetic nerve stimulation on vasoconstrictor responses and overflow of norepinephrine (NE) and neuropeptide Y-like immunoreactivity (NPY-LI) were studied in the dog gracilis muscle and pig spleen in vivo. A continuous regular impulse activity was compared with irregular human sympathetic and regular bursting patterns. During control conditions, stimulation with the irregular activity induced larger peak vasoconstriction than the regular activity at 0.59 Hz, but not at higher frequencies in the muscle, at 0.59 and 2.0 Hz in the spleen. The nerve stimulation-evoked overflow of NE and NPY-LI from the muscle were not influenced by the pattern of stimulation. The overflow of NPY-LI, but not that of NE, from the spleen was enhanced by the irregular activity at 0.59 and 2.0 Hz, and both NPY-LI and NE overflows were enhanced by regular burst activity at 2.0 Hz. After blockade of alpha- and beta-adrenoceptors by phenoxybenzamine and propranolol, respectively, which enhanced nerve stimulation-evoked overflow of both NE and NPY-LI, the NE overflow from the muscle evoked by the irregular activity was slightly larger at 0.59 Hz but smaller at higher frequencies compared with that evoked by regular activity, whereas the detectable overflow of NPY-LI was not largely influenced by the stimulation pattern. In conclusion, both the vasoconstrictor response and the overflow of NPY-LI and NE seem to be influenced by the pattern and frequency of sympathetic nerve stimulation.


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