Ion transport across plasma membrane in primary hypertension

Postnov, Yu. V.; Orlov, Sergei N.

doi:10.1152/physrev.1985.65.4.904

Cited by 127 publications

(28 citation statements)

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“…Numerous ion transport abnormalities are associated with human and experimental hypertension (1)(2)(3)(4)(5). Altered activity of the Na -K pump and/or Na -K cotransport system (HTG) (15,16).…”

Section: Introductionmentioning

confidence: 99%

Membrane Ion Transport in Erythrocytes of Salt Hypertensive Dahl Rats and Their F2 Hybrids: the Importance of Cholesterol

Vokurková¹,

Dobešová²,

Kuneš³

et al. 2003

Hypertens Res

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The possible association of salt hypertension and altered lipid metabolism with abnormalities of particular systems transporting sodium and potassium has been studied in erythrocytes of Dahl rats and their F2 hybrids fed a high-salt diet since weaning. Our attention was paid to the Na -K pump, Na -K cotransport and especially to passive membrane permeability for Na and Rb (Na and Rb leak), because the Na leak was found to be dependent on the genotype, age and salt intake of Dahl rats, whereas the Rb leak was sug-

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Section: Introductionmentioning

confidence: 99%

Membrane Ion Transport in Erythrocytes of Salt Hypertensive Dahl Rats and Their F2 Hybrids: the Importance of Cholesterol

Vokurková¹,

Dobešová²,

Kuneš³

et al. 2003

Hypertens Res

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“…In the latter, marked discrepancies characterized the results of various clinical investigations. 2 Much of this variability in the data can be accounted for by methodological problems. The flux studies were performed by measuring transport activity under a fixed experimental condition, although Na + transport is a complex function of the concentrations of substrates and effectors, particularly of cell Na + content.…”

mentioning

confidence: 99%

Sodium transport kinetics in erythrocytes from spontaneously hypertensive rats.

1988

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SUMMARY Rat erythrocytes with five different amounts of Na+ content have been prepared by using a new, nondetrimental Na+-loading method (net NaHPO 4 " influx through the anion carrier). This method allowed the determination of 1) maximal translocation rates and apparent dissociation constants for internal Na+ of the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport and 2) rate constants of Na+ leak in erythrocytes from spontaneously hypertensive rats of the Okamoto strain and Wistar-Kyoto normotensive controls aged 2 to 26 weeks. Two major abnormalities were found in erythrocytes from spontaneously hypertensive rats: 1) a decreased cotransport affinity for internal Na +, which was constantly observed from 2 to 26 weeks of age (mean intracellular Na+ content for half-maximal stimulation of outward Na+-K+ cotransport = 33.1 ± 7.0 [SD] mmol/L cells in spontaneously hypertensive rats vs 16.7 ± 4.7 mmol/L cells in Wistar-Kyoto rats; p<0.001), and 2) a decreased maximal pump rate in adult (15-to 26-week-old) spontaneously hypertensive as compared with that for age-matched Wistar-Kyoto rats (9-37 vs 34-70 mmol/L cells/hr). Therefore, the low cotransport affinity for internal Na+ appears to be a stable, possibly genetic defect of spontaneously hypertensive rats. Conversely, the decreased maximal pump rate may be a secondary event, possibly reflecting the appearance of endogenous pump inhibitors in the plasma of adult spontaneously hypertensive rats. (Hypertension 11: 41-48, 1988) KEY WORDS • ion transport • sodium transport • hypertension • membranes erythrocyte • rats • spontaneously hypertensive rats E PIDEMIOLOGICAL, clinical, and experimental studies have suggested that an inborn error of Na + metabolism is involved in the pathogenesis of primary hypertension.1 This hypothesis has been extensively investigated by measuring Na + content and Na + flux in circulating cells from rats and humans with primary hypertension (for a review, see Reference 2). The results were very difficult to interpret in both animals and humans. In the former, abnormal cell Na + handling was frequently observed, but the nature of the transport alteration differed markedly among different strains (see, for instance, Reference 3). In the latter, marked discrepancies characterized the results of various clinical investigations.2 Much of this variability in the data can be accounted for by methodological problems. The flux studies were performed by measuring transport activity under a fixed

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“…An altered state of vascular reactivity can result from alterations in either cellular calcium me tabolism or the sensitivity of response elements to the actions of Ca 2+ . 7 " 10 Investigations in search of support for the hypothesis that perturbation of calcium metabo lism is a fundamental lesion in EHT have been carried out on a wide variety of tissue and cell types including myocardium, smooth muscle, erythrocytes, adipocytes, hepatocytes, synaptosomes, and platelets in both human and animal models of hypertension.…”

Section: Essential Hypertension Platelets and Calciummentioning

confidence: 99%

Platelet Membrane and Calcium Control Abnormalities in Essential Hypertension

Tj²

1988

American Journal of Hypertension

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Ion transport across plasma membrane in primary hypertension

Cited by 127 publications

References 0 publications

Membrane Ion Transport in Erythrocytes of Salt Hypertensive Dahl Rats and Their F2 Hybrids: the Importance of Cholesterol

Membrane Ion Transport in Erythrocytes of Salt Hypertensive Dahl Rats and Their F2 Hybrids: the Importance of Cholesterol

Sodium transport kinetics in erythrocytes from spontaneously hypertensive rats.

Platelet Membrane and Calcium Control Abnormalities in Essential Hypertension

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