Ion transport systems in erythrocyte membrane of spontaneously hypertensive rats (SHR) as compared with normotensive rats of the Brown Norway (BN.lx) strain.

The activity of Na+, K(+)-ATPase in SHR erythrocytes treated with saponin is increased by 30-40% as compared to the Brown Norway (BN.lx) strain whereas the activity of Ca(2+)-ATPase is decreased by 20-30%. Passive permeability of SHR erythrocytes determined by 86Rb influx is increased by 20-30%.

Na+/H+ exchange in erythrocytes of spontaneously hypertensive rats: a study in F2 SHR x WKY hybrids.

The rate of proton gradient-induced Na+/H+ exchange in the erythrocytes of SHR was increased by 50-60% as compared to WKY animals. No significant correlation between Na+/H+ exchange and blood pressure was revealed in F2 hybrids of SHR and WKY rats. Na+/H+ exchange rate in the erythrocytes of F2 SHR x WKY hybrids was twice as high as in SHR and three times higher than in WKY rats.

Protein kinase C activity in erythrocytes in primary hypertension: regulation of cell shape and cation transport.

Protein kinase C activity in the lysate of erythrocytes of patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR) was found to be increased by 1.6-2.0 times as compared with normotensive controls.

Volume-dependent regulation of cation transport and polyphosphoinositide metabolism in human and rat erythrocytes: features revealed in primary hypertension.

The rate of delta mu H+ --induced erythrocyte Na+/H+ exchange is increased in both patients with essential hypertension (EH) and spontaneously hypertensive rats (SHR). The increase of Na+,K(+)-cotransport was revealed in erythrocytes of SHR only. This alteration as well as a decrease of mean cell volume were observed in both young and old erythrocytes of SHR.

Erythrocyte membrane sialic acids in primary and secondary hypertension in man and rat.

Sialic acids of erythrocyte membranes (erythrocyte 'ghosts') and blood plasma were studied in patients with essential or chronic renal hypertension, and in spontaneously hypertensive rats (SHR). The total content of sialic acids in erythrocyte membranes (determined by thiobarbituric-acid assay) was around 100 mumol/g protein in both the hypertensive patients and controls, there being no difference between the three groups. Similarly total sialic-acid content of plasma did not differ between the hypertensive patients and controls, being around 2 mmol/l.

Calmodulin distribution and Ca2+ transport in the erythrocytes of patients with essential hypertension.

The rate of calcium transport and calmodulin distribution in the erythrocytes of patients with essential hypertension were studied. In erythrocyte membranes subjected to calmodulin depletion by treatment with EGTA, both the affinity of the calcium pump for Ca2+ and its maximal activity were the same in normotensive and hypertensive patients. The addition of exogenous calmodulin to calmodulin-stripped membranes from erythrocytes of patients with essential hypertension resulted in a smaller increase of the maximal activity of the calcium pump and its affinity for Ca2+.

Calcium transport and protein content in cell plasma membranes of spontaneously hypertensive rats.

In the absence of depolarizing agents, 45Ca uptake by synaptosomes of the brain tissue of spontaneously hypertensive rats (SHR) was 40% greater than in normotensive controls. This difference disappeared after membrane treatment with depolarizing agents or with the addition of the Ca channel blocker verapamil. Increased 45Ca uptake was also observed in isolated platelets of SHR.

Calcium transport in synaptosomes and subcellular membrane fractions of brain tissue in spontaneously hypertensive rats.

The uptake of Na+ and Ca2+ by synaptosomes and uptake of Ca2+ by the mitochondria and microsomes of brain tissue of rats with spontaneous hypertension (SH rats) and normotensive Kyoto-Wistar rats (WKY rats) were studied with an isotope-exchange method. By means of inhibitor analysis it has been shown that calcium influx into the synaptosomes during depolarization of their plasma membrane takes place only through the potential-dependent channels in both groups of animals. Basal Ca2+ uptake by the synaptosomes of hypertensive rats was increased, apparently by partial depolarization of the synaptosome membrane caused by the increased membrane permeability to Na+ (basal Na+ uptake by synaptosomes was found to be increased in hypertensive rats).

Calmodulin-dependent Ca2+ transport in erythrocytes of spontaneously hypertensive rats.

Ca2+ transport in inside-out vesicles of the erythrocyte membranes of spontaneously hypertensive rats (SHR) was studied. In the presence of calmodulin, the rate of 45Ca uptake by the erythrocyte membranes of SHR was half that of erythrocyte membranes of the normotensive control group. It is suggested that the decrease of the rate of calmodulin-dependent calcium transport across the plasma membrane may be a cause for the increased intracellular calcium content found in some tissues of spontaneously hypertensive rats in previous studies.

Evidence of altered structure of the erythrocyte membrane in spontaneously hypertensive rats.

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.

Alteration of the intracellular calcium pool of adipose tissue in spontaneously hypertensive rats. No effect of peripheral immunosympathectomy.

The intracellular calcium pool of adipose tissue was estimated by studying the kinetics of 45Ca efflux from the tissue of 9-week old spontaneously hypertensive (SHR) and normotensive Kyoto-Wistar (NKWR) rats subjected to peripheral immunosympathectomy (nerve growth factor antiserum treatment of newborn rats) and in intact (sham-treated) animals of both strains. The development of hypertension in SHR was prevented by immunosympathectomy, however, both groups, SHR-intact and immunosympathectomized rats showed an increase in the intracellular calcium content of adipocytes. These results indicate that the alteration of the membrane control over intracellular calcium distribution in adipose tissue of SHR cannot be attributed to an enhanced activity of the sympathetic nervous system.