Vascular Sodium—Potassium Pump Activity in Various Models of Experimental Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 179s-181s ◽  
Author(s):  
M. B. Pamnani ◽  
D. L. Clough ◽  
S. J. Huot ◽  
F. J. Haddy
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cell Membrane Permeability ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Primary Defect ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Sodium Potassium Pump

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.

Evidence of Altered Permeability of the Erythrocyte Membrane for Sodium and Potassium ions in Spontaneously Hypertensive Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 169s-172s ◽  
Author(s):  
YU. V. Postnov ◽  
S. N. Orlov ◽  
P. V. Gulak ◽  
A. S. Shevchenko
Keyword(s):  
Erythrocyte Membrane ◽  
Spontaneously Hypertensive Rats ◽  
Potassium Ions ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Sodium Potassium Pump ◽  
Sodium And Potassium

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.

scholarly journals The effects of pertussis toxin-treatment on integrated vasoactive response of vascular system in spontaneously hypertensive rats

2008 ◽  
pp. 137-139
Author(s):  
S Čačányiová ◽  
F Kristek ◽  
J Kuneš ◽  
J Zicha
Keyword(s):  
Pertussis Toxin ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Vascular System ◽  
Pressor Response ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Right ◽  
Hypotensive Response

We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteenweek-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 µg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTXsensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension.

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