scholarly journals Intrinsic difference in erythrocyte membrane in spontaneously hypertensive rats characterized by Na+ and K+ fluxes

1983 ◽  
Vol 399 (1) ◽  
pp. 74-78 ◽  
Author(s):  
Cosmas J. M. van de Ven ◽  
David F. Bohr
1982 ◽  
Vol 63 (s8) ◽  
pp. 37s-39s ◽  
Author(s):  
P. Marche ◽  
S. Koutouzov ◽  
P. Meyer

1. The distribution and metabolism of inositol phospholipids were studied in the erythrocyte membrane of spontaneously hypertensive and normotensive Wistar-Kyoto rats. The incorporation of 32P into these lipids was considered as an index of their turnover, and a reflection of their metabolism. 2. With [γ-32P]ATP as the source of label only the polyphosphoinositides (diphosphoinositide and triphosphoinositide) incorporated 32P. The levels of labelling were lower in hypertensive than in normotensive rats. Our data indicate that, in the hypertensive rats, the kinases responsible for the labelling of polyphosphoinositides exhibited decreased Vmax. for ATP. 3. These changes may be related to those described for calcium binding and transport in the erythrocyte of spontaneously hypertensive rats.


1982 ◽  
Vol 63 (1) ◽  
pp. 43-45 ◽  
Author(s):  
S. N. Orlov ◽  
P. V. Gulak ◽  
I. S. Litvinov ◽  
YU. V. Postnov

1. The membrane structure of erythrocytes of rats with different forms of arterial hypertension was studied by means of two hydrophobic fluorescent probes (diphenylhexatriene and pyrene). 2. Microviscosity of hydrophobic areas of erythrocyte membrane of spontaneously hypertensive rats was found to be increased compared with that of membranes from normotensive control rats. 3. No alterations of membrane structure of erythrocytes of deoxycorticosterone-treated rats and renal hypertensive rats were found.


1980 ◽  
Vol 59 (s6) ◽  
pp. 207s-209s ◽  
Author(s):  
S. N. Orlov ◽  
Yu. V. Postnov

1. The ability of isolated membrane fractions of cardiomyocytes, aortic smooth muscle and erythrocytes from spontaneously hypertensive rats to bind calcium was investigated isotopically. 2. Plasma membranes of aortic smooth muscle and erythrocytes of spontaneously hypertensive rats possess a lower calcium-binding ability than preparations from normotensive controls. 3. Sarcoplasmic reticulum from the myocardium of spontaneously hypertensive rats had a lower ability to accumulate calcium. 4. Changes in the calcium-binding ability of the erythrocyte membrane of spontaneously hypertensive rats was related to the diminution of the amount of exchangeable calcium on the inner part of the membrane. The latter may be the cause of the increase of erythrocyte membrane permeability for sodium in spontaneously hypertensive rats and in patients with essential hypertension.


1984 ◽  
Vol 2 (1) ◽  
pp. 81-84 ◽  
Author(s):  
Pavel V. Gulak ◽  
Sergei N. Orlov ◽  
Nikolai I. Pokudin ◽  
Yuvenali V. Postnov ◽  
Ivan S. Litvinov ◽  
...  

2018 ◽  
Vol 17 (4) ◽  
pp. 103-109
Author(s):  
A. V. Nosarev ◽  
Yu. G. Birulina ◽  
I. V. Petrova ◽  
I. V. Kovalev ◽  
S. V. Gusakova ◽  
...  

Aim.To study the ionic mechanisms which underlie regulation contractile activity of vascular smooth muscles and the erythrocytes membrane potential from spontaneously hypertensive rats.Materials and methods.The effect of acetylcholine (ACX), 10 μM, and Ca2+ -ionophore A23187, 10 μM, on the contractile reactions of isolated smooth muscle segments of the aorta from 11-week-old spontaneously hypertensive rats (SHR) and Wistar – Kyoto rats (WKY) induced by phenylephrine (PE), 1 μM, was measured by the mechanography. 11-week-old SHR were divided into control and experimental groups depending on the drug administration (amlodipine 10 mg/kg given intragastrically). Blood pressure (BP) in SHR was measured before and after treatment. The amplitude of the hyperpolarizating response (HO) and the activity of Ca2+-dependent K+-channels of the erythrocyte membrane of SHR were performed with potentiometric method.Results.In response to the stimulating effect of the ACX or the calcium ionophore A23187, the smooth muscle segments of the aorta from the WKY and SHR precontracted with PE were relaxed. To the addition of the ACX, the vascular segments of the SHR responded with a stronger dilatation than the WKY segments, but not the action of the Ca2+-ionophore. Treatment of SHR with blocker of Ca2+-channels of L-type amlodipine caused a decrease the BP, and an increase in the relaxing effect of intact aortic segments on the ACX and Ca2+-ionophore. There was an increase the amplitude of HO and activity of Ca2+-dependent K+-channels of the erythrocyte membrane from SHR.Conclusion.Relaxation of vascular smooth muscle in SHR is caused by changes in the endothelial function and Ca2+-dependent ionic conductivity of the myocyte membrane. An increase of the hyperpolarizating response of the erythrocyte membrane from rats with spontaneous hypertension is associated with activation of potassium channels. The selective effect on these intracellular targets can serve as a basis for the development of antihypertensive drugs.


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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