scholarly journals Calcium sensitivity of Ca2(+)-activated K+ channels in spontaneously hypertensive stroke-prone rats.

Hypertension ◽  
1990 ◽  
Vol 15 (2_Suppl) ◽  
pp. I97-I97 ◽  
Author(s):  
P. B. Furspan ◽  
D. F. Bohr
1994 ◽  
Vol 113 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Eneida G. Silva ◽  
Eugenio Frediani-Neto ◽  
Alice T. Ferreira ◽  
Antonio CM. Paiva ◽  
Therezinha B. Paiva

2002 ◽  
Vol 29 (7) ◽  
pp. 575-581 ◽  
Author(s):  
Masahiro Kamouchi ◽  
Takanari Kitazono ◽  
Tetsuhiko Nagao ◽  
Masatoshi Fujishima ◽  
Setsuro Ibayashi

1980 ◽  
Vol 59 (s6) ◽  
pp. 203s-205s ◽  
Author(s):  
M. J. Mulvany ◽  
N. Nyborg ◽  
H. Nilsson

1. We have investigated the noradrenaline-activated calcium sensitivity of 150 μm mesenteric resistance blood vessels from spontaneously hypertensive and control Wistar-Kyoto rats. 2. Under control conditions the spontaneously hypertensive rat blood vessels had a greater calcium sensitivity than the Wistar-Kyoto rat vessels. 3. In the presence of 1 mmol of ouabain/l, a treatment known to inhibit the sodium-potassium-dependent ATPase, the responses of the spontaneously hypertensive rat blood vessels were reduced more than those of the Wistar-Kyoto rat blood vessels, so that the responses of spontaneously hypertensive rat and Wistar-Kyoto rat blood vessels were then similar. 4. Similar results were obtained by removing external potassium, a procedure which should also inhibit the sodium-potassium-ATPase. 5. The results suggest that the greater noradrenaline-activated calcium sensitivity of spontaneously hypertensive rat blood vessels may be associated with an increased sodium-potassium-ATPase activity.


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