Isolation and characterization of clonal vascular smooth muscle cell lines from spontaneously hypertensive and normotensive rat aortas

1991 ◽  
Vol 27 (10) ◽  
pp. 791-798 ◽  
Author(s):  
Keith L. Hall ◽  
Joseph W. Harding ◽  
Howard L. Hosick
Cells ◽  
2016 ◽  
Vol 5 (3) ◽  
pp. 36
Author(s):  
Pamela Lazar-Karsten ◽  
Gazanfer Belge ◽  
Detlev Schult-Badusche ◽  
Tim Focken ◽  
Arlo Radtke ◽  
...  

1997 ◽  
Vol 73 ◽  
pp. 203
Author(s):  
Masuda Tsuyoshi ◽  
Ohmi Kazuhiro ◽  
Yamaguchi Hideki ◽  
Matsuda Yuzuru ◽  
Iino Masamitsu ◽  
...  

Cells ◽  
2016 ◽  
Vol 5 (2) ◽  
pp. 19 ◽  
Author(s):  
Pamela Lazar-Karsten ◽  
Gazanfer Belge ◽  
Detlev Schult-Badusche ◽  
Tim Focken ◽  
Arlo Radtke ◽  
...  

2015 ◽  
Vol 35 (7) ◽  
pp. 1127-1136 ◽  
Author(s):  
Jennifer A Iddings ◽  
Ki Jung Kim ◽  
Yiqiang Zhou ◽  
Haruki Higashimori ◽  
Jessica A Filosa

Functional hyperemia is the regional increase in cerebral blood flow upon increases in neuronal activity which ensures that the metabolic demands of the neurons are met. Hypertension is known to impair the hyperemic response; however, the neurovascular coupling mechanisms by which this cerebrovascular dysfunction occurs have yet to be fully elucidated. To determine whether altered cortical parenchymal arteriole function or astrocyte signaling contribute to blunted neurovascular coupling in hypertension, we measured parenchymal arteriole reactivity and vascular smooth muscle cell Ca2+ dynamics in cortical brain slices from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We found that vasoconstriction in response to the thromboxane A2 receptor agonist U46619 and basal vascular smooth muscle cell Ca2+ oscillation frequency were significantly increased in parenchymal arterioles from SHR. In perfused and pressurized parenchymal arterioles, myogenic tone was significantly increased in SHR. Although K+-induced parenchymal arteriole dilations were similar in WKY and SHR, metabotropic glutamate receptor activation-induced parenchymal arteriole dilations were enhanced in SHR. Further, neuronal stimulation-evoked parenchymal arteriole dilations were similar in SHR and WKY. Our data indicate that neurovascular coupling is not impaired in SHR, at least at the level of the parenchymal arterioles.


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