Different ratio of myosin heavy chain isoforms in arterial smooth muscle of spontaneously hypertensive rats

1990 ◽  
Vol 85 (2) ◽  
pp. 209-216 ◽  
Author(s):  
M. P. Sparrow ◽  
H. W. Mitchell ◽  
A. W. Everett
1994 ◽  
Vol 74 (3) ◽  
pp. 167-173 ◽  
Author(s):  
Heikki Wuorela ◽  
Pertti Arvola ◽  
Mika Kähönen ◽  
Heikki Vapaatalo ◽  
Ilkka Pörsti

1993 ◽  
Vol 108 (4) ◽  
pp. 980-990 ◽  
Author(s):  
Pertti Arvola ◽  
Heikki Ruskoaho ◽  
Heikki Wuorela ◽  
Anu Pekki ◽  
Heikki Vapaatalo ◽  
...  

1988 ◽  
Vol 66 (12) ◽  
pp. 1513-1517
Author(s):  
C. S. Packer ◽  
M. L. Kagan ◽  
R. A. Meiss ◽  
N. L. Stephens

Both isometric and isotonic relaxation rates have previously been reported to be decreased in caudal arterial and mesenteric resistance arterial smooth muscle from 16- to 21-week-old spontaneously hypertensive rats (SHR) compared with muscle from age-matched normotensive Wistar–Kyoto rats (WKY). An increased maximum velocity of shortening (Vmax) and an increased shortening ability (ΔLmax) have also been reported for arterial smooth muscle from 16- to 21-week-old SHR. It has been suggested that both increased narrowing and prolonged narrowing of arteries contribute to the development of hypertension. However, SHR Vmax is not different from WKY Vmax when studying arterial muscle from older (28- to 31-week-old) rats. Thus increased arterial narrowing ability cannot be a contributing factor to the maintenance of hypertension. In this study the role of relaxation rate in the maintenance of hypertension was examined by comparing the relaxation rates of isometric and isotonic contractions of caudal arterial strips from 16- to 21-week-old SHR (n = 9) and WKY (n = 8) and from 28- to 31-week-old SHR (n = 7) and WKY (n = 5). While relaxation rates were lower for 16- to 21-week-old SHR compared with age-matched WKY preparations for both isometric and isotonic contractions, only isometric relaxation rates were found to be different in 28- to 31-week-old SHR compared with 28- to 31-week-old caudal arterial muscle (p < 0.05). Vmax tended to normalize from a once-elevated velocity, while isometric relaxation rate remained decreased in SHR with ageing and (or) with progression of the hypertensive condition. Therefore, slower relaxation, but not increased shortening ability, may contribute to the maintenance of high blood pressure in this genetic model of essential hypertension. A decreased Ca2+ resequestering rate or slower Ca2+ extrusion from the cell or decreased phosphatase activity are some of the possible candidates for the slow relaxation reported for the hypertensive arterial smooth muscle.


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