Erythrocyte ion transport alterations in hypertriglyceridaemic rats.

1. Hypertension appears to be associated with both abnormalities in ion transport and disturbances in lipid metabolism. The aim of the present study was to search for alterations in erythrocyte ion transport in hereditary hypertriglyceridaemic rats. This strain is characterized by a pronounced elevation of blood pressure which correlates with the plasma triacylglycerol level. 2. Erythrocyte Na+ content was elevated in hypertriglyceridaemic rats due to an increased ouabain-resistant Na+ net uptake. This was caused not only by the acceleration of bumetanide-sensitive Na+ inward co-transport, but also by the augmentation of bumetanide-resistant Na+ inward leak. A moderate enhancement of bumetanide-sensitive Rb+ uptake was seen in hypertriglyceridaemic animals, but there were no changes in bumetanide-resistant Rb+ leak. 3. The plasma triacylglycerol level correlated positively not only with blood pressure (P < 0.001) but also with ouabain-resistant Na+ transport (P < 0.002), bumetanide-sensitive Na+ and K+ (Rb+) co-transport (P < 0.01 and P < 0.001, respectively), bumetanide-resistant Na+ leak (P < 0.02) and erythrocyte Na+ content (P < 0.05). 3. Thus the association of augmented ouabain-resistant Na+ transport with elevated blood pressure in this form of experimental hypertension might be mediated by genetic disorders of lipid metabolism.

Red cell ouabain-resistant Na+ and K+ transport in Wistar, brown Norway and spontaneously hypertensive rats.

Our previous studies concerning the role of furosemide-resistant cation leaks in genetic hypertension demonstrated that blood pressure of recombinant inbred strains (derived from F2 hybrids of spontaneously hypertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measured in Mg(2+)-sucrose medium) or with Rb+ uptake (found in either medium). In the present study the alterations of particular components of ouabain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na(+)-free (Mg(2+)-sucrose or choline) incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains--Brown Norway and Wistar rats. This was mainly due to an increased bumetanide-resistant (BR) Na+ inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythrocytes were seen not only in Mg(2+)-sucrose medium but also in choline medium. In both Na(+)-free media there was a considerable saturable Na+i-dependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the interpretation of the data on "increased passive membrane permeability" obtained in SHR erythrocytes incubated in Na(+)-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na(+)-K+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Red cell ouabain-resistant Na+ and K+ transport in Wistar, Brown Norway and spontaneously hypertensive rats.

Our previous studies concerning the role of furosemide-resistant cation leaks in genetic hypertension demonstrated that blood pressure of recombinant inbred strains (derived from F2 hybrids of spontaneously hypertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measured in Mg(2+)-sucrose medium) or with Rb+ uptake (found in either medium). In the present study the alterations of particular components of ouabain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na(+)-free (Mg(2+)-sucrose or choline) incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains--Brown Norway and Wistar rats. This was mainly due to an increased bumetanide-resistant (BR) Na+ inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythrocytes were seen not only in Mg(2+)-sucrose medium but also in choline medium. In both Na(+)-free media there was a considerable saturable Na+i-dependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the interpretation of the data on "increased passive membrane permeability" obtained in SHR erythrocytes incubated in Na(+)-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na(+)-K+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Complete dissociation of DOCA-salt hypertension and red cell ion transport alterations.

Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.

Potassium influx into erythrocytes in essential hypertension.

Sodium plus potassium (Na+K) cotransport in erythrocytes of patients with essential hypertension has mainly been studied elsewhere by measuring net outward frusemide-sensitive Na and K movements. We compared K influx (tracer 86 Rubidium) in control subjects and hypertensives who had never previously been treated for hypertension. The cotransport K influx rates in controls and hypertensives were 0.44 +/- 0.02 (mumol/ml cells/h; mean +/- s.e.; n = 20) and 0.67 +/- 0.06 (mumol/ml cells/h; mean +/- s.e.; n = 23) respectively. The active influxes were 1.03 +/- 0.03 and 2.06 +/- 0.13 (mumol/ml cells/h; mean +/- s.e.) respectively. The variance of both parameters was significantly greater in the hypertensive group but, taking this into account, the differences were significant (P less than 0.01).