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(Hypertension. 1997;30:636.)
© 1997 American Heart Association, Inc.

Articles

Plasma Triglycerides and Red Cell Ion Transport Alterations in Genetically Hypertensive Rats

Josef Zicha; Zdenka Dobesová; Jaroslav Kunes

From the Institute of Physiology, Academy of Sciences of the Czech Republic, Prague.

Abstract Ion transport abnormalities in essential hypertension are often associated with concomitant changes of lipid metabolism, but this information is missing in rats with genetic hypertension. We therefore studied the alterations of red cell Na⁺ and K⁺ transport and their relationship to blood pressure and plasma lipids (cholesterol and triglycerides) in Prague hereditary hypertriglyceridemic (HTG) rats, Lyon hypertensive (LH) rats, and HTGxLewis F₂ hybrids. In both hypertensive models and F₂ hybrids, red cell Na⁺ content (Na⁺_i) was positively related to plasma triglycerides but not to plasma cholesterol levels. Na⁺_i elevation was more pronounced in HTG than in LH rats, probably due to higher plasma triglycerides in the former strain. The two hypertensive strains differed in bumetanide-sensitive Na⁺ transport, which was augmented in HTG rats with low plasma cholesterol but suppressed in LH rats characterized by high cholesterol levels. In the two genetic models, there was a positive association of blood pressure with Na⁺ leak, and this was also confirmed by the cosegregation of these parameters in F₂ hybrids. We conclude that the enhancement of Na⁺ leak represents the major ion transport abnormality in rats with genetic hypertension. The alterations in plasma lipids are important determinants of abnormal red cell ion transport in hypertensive models studied. Although the detailed mechanism of their participation in ion transport regulation is still not completely understood, triglyceride-dependent changes in membrane microviscosity seem to be responsible for the modulation of particular ion transport pathways.

Key Words: blood pressure • erythrocytes • Na⁺-K⁺ cotransport • Na⁺-K⁺ pump • plasma triglycerides • plasma cholesterol

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