Sodium-Potassium Pump Sites, as Assessed by [3H]-Ouabain Binding, in Aorta and Caudal Artery of Normotensive and Spontaneously Hypertensive Rats

1984 ◽  
Vol 21 (5) ◽  
pp. 211-222
Author(s):  
Stanley K. Wong ◽  
David P. Westfall ◽  
Dennis Menear ◽  
William W. Fleming
1980 ◽  
Vol 59 (s6) ◽  
pp. 179s-181s ◽  
Author(s):  
M. B. Pamnani ◽  
D. L. Clough ◽  
S. J. Huot ◽  
F. J. Haddy

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension. 2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension. 3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.


1976 ◽  
Vol 51 (s3) ◽  
pp. 169s-172s ◽  
Author(s):  
YU. V. Postnov ◽  
S. N. Orlov ◽  
P. V. Gulak ◽  
A. S. Shevchenko

1. Erythrocyte membrane permeability to sodium and potassium ions was studied in 8–10 weeks spontaneously hypertensive rats (SHR, Kyoto/Wistar strain), normotensive Wistar and Sprague—Dawley rats. 2. The rate of 22Na efflux from the erythrocytes and the rate constant of Na/Na exchange were considerably greater in SHR than in normotensive Wistar and Sprague—Dawley rats. This difference remained the same in rats adrenalectomized 7 days before the experiment. The maximum difference in the constants was found when the sodium—potassium pump was blocked by ouabain. 3. The accumulation of 42K in the erythrocytes of SHR (the sodium—potassium pump being blocked) took place at a considerably slower rate, and the K+ wash-out into a potassium-free medium was faster than that in the normotensive Wistar and Sprague—Dawley rats. 4. These results indicate a higher permeability of the erythrocyte membrane of SHR for Na+ and K+, compared with normotensive Wistar and Sprague—Dawley strains. It is suggested that this may reflect a more widespread cell-membrane defect, which could serve as a general cause for activating the mechanisms maintaining high blood pressure.


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