Na+-H+ exchange and other ion-transport systems in erythrocytes of essential hypertensives and spontaneously hypertensive rats: a comparative analysis

Sn, Orlov; Iy, Postnov; Ni, Pokudin; Vy, Kukharenko; Yv, Postnov

doi:10.1097/00004872-198910000-00003

Cited by 58 publications

(16 citation statements)

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“…Nevertheless, it should be noted that pH i in resistance arteries of SHR was increased only in young, 5-week-old, but not in adult, 12-week-old, animals 203 ; increased pH i in resistance arteries of adult SHR was only observed in absence of bicarbonate 205 ; and higher pH i seen initially in cultured VSMC from SHR disappeared after several passages. 204 In contrast to the scarce information about the activity of HCO 3 Ϫ /Cl Ϫ exchangers in genetic hypertension, 197,208 Na ϩ /H ϩ exchanger activity is increased in various blood cells 179,209,210 and cultured VSMC of SHR. 202,207,211 The enhanced rate of Na ϩ /H ϩ exchange in SHR is ascribed to increased V max , whereas further kinetic alterations of the Na ϩ /H ϩ exchanger are still uncertain.…”

Section: /Clmentioning

confidence: 94%

Abnormalities of membrane function and lipid metabolism in hypertension A review

Zicha

Kuneš

Devynck

1999

American Journal of Hypertension

208

175

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Hypertension, which is characterized by multiple alterations in the structure and function of the cell membrane, is often associated with important metabolic abnormalities including those concerning lipid metabolism. Dyslipidemia accompanying essential hypertension consists of elevated plasma triglycerides, low HDL cholesterol, and increased levels of atherogenic LDL cholesterol particles. The altered membrane microviscosity seen in hypertensive subjects reflects the changes of membrane lipid composition resulting from intensive exchange between circulating and membrane lipids, as well as from abnormal cellular lipid synthesis and metabolism. The changes of membrane microviscosity are known to modulate the activity of proteins involved in ion transport, signal transduction, cell Ca 2؉ handling, intracellular pH regulation, etc. Alterations in plasma or membrane lipids are indeed closely associated with ion transport abnormalities as well as with impaired control of cytosolic Ca 2؉ T here is no doubt that essential hypertension is associated with multiple membrane alterations, including changes in membrane microviscosity, receptor function, signal transduction, ion transport, calcium mobilization, intracellular pH regulation, and so on. Lipids, as an integral part of the cell membrane, play a decisive role in the modulation of the membrane properties mentioned. Specific lipid-lipid and lipid-protein interactions result in a highly dynamic but precisely controlled architecture of membrane components. Major regulators of membrane architecture are membrane potential, intracellular Ca 2ϩ and pH, lipid composition, cell-to-cell contact, and membrane coupling with the cytoskeleton or extracellular matrix. Intermolecular associations in the membrane and at the membrane-cytoskeleton interface are further selectively controlled by specific phosphorylation and dephosphorylation cascades involving both proteins and lipids. This is regulated by the extracellular matrix as well as by the binding of growth factors and hormones to their specific receptors. 1,2The aim of this review is to outline some interrelationships between abnormal lipid metabolism and altered membrane structure or function in human and experimental hypertension, and to evaluate whether abnormal lipid metabolism, which is responsible for a great part of membrane abnormalities found in hypertension, might be an integral part of its pathogenetic mechanisms. BLOOD PRESSUREMultiple metabolic abnormalities often accompany essential hypertension. Decreased high-density lipoproteins (HDL) together with increased plasma levels of low-density (LDL) and very low-density lipoproteins (VLDL), as well as hypertriglyceridemia, hypercholesterolemia, and insulin resistance, were found in many hypertensive patients. 3,4 There is increasing evidence for a genetic basis for the association of hypertension with insulin resistance and dyslipidemia. The genetic locus associated with dyslipidemia accompanying hypertension or diabetes seems to be closely linked to the LDL recept...

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Section: /Clmentioning

confidence: 94%

Abnormalities of membrane function and lipid metabolism in hypertension A review

Zicha

Kuneš

Devynck

1999

American Journal of Hypertension

208

175

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“…-activated K + channels [14] served as positive controls in this study. Blood was collected from anesthetized Wistar rats in tubes containing 20 U/ml heparin and sedimented (5,000 rpm, 10 min).…”

Section: +mentioning

confidence: 99%

“…E m was measured as the transmembrane gradient of H + in the presence of the protonophore CCCP, as described previously [14,17]. Briefly, 150 µl of packed erythrocytes were added to 2.5 ml of medium containing 150 mM NaCl, 1 mM KCl, 1 mM MgCl 2 , 10 mM D-glucose, 0.5 mM CaCl 2 and 20 µM CCCP with the additions listed in Table 4.…”

Section: Measurement Of Free Intracellular Camentioning

confidence: 99%

Swelling-Induced K<sup>+</sup> Fluxes in Vascular Smooth Muscle Cells are Mediated by Charybdotoxin-Sensitive K<sup>+</sup> Channels

Anfinogenova

Rodrı́guez

Grygorczyk

et al. 2001

Cell Physiol Biochem

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This study examines the relative contributions of K-Cl cotransport and K⁺ channels to swelling-induced K⁺ fluxes in vascular smooth muscle cells (VSMC). DIOA known as a potent inhibitor of erythrocyte K-Cl cotransport exerts diverse side-effects on VSMC and can not be used to analyze the role of this carrier in swelling-induced K⁺ fluxes. Other inhibitors of K-Cl cotransport (furosemide, okadaic acid and calyculin A) did not affect K⁺ fluxes in VSMC triggered by swelling. Swelling-induced K⁺ fluxes in VSMC were also not affected by K⁺ channel blockers such as TEA, glibenclamide and apamin, but were blocked by Ba²⁺ and charybdotoxin (ChTX), a potent inhibitor of Ca²⁺- and voltage-gated K⁺ channels. Swelling-induced K⁺ influx in VSMC was diminished in Ca²⁺-free medium and in cells loaded with Ca²⁺ chelator BAPTA, but was not accompanied by detectable elevation of [Ca²⁺]_i. In contrast to Ca²⁺-induced hyperpolarization of erythrocytes triggered by activation of intermediate conductance Ca²⁺-gated K⁺ channels (IK_Ca), neither clotrimazole nor calmodulin antagonists (R24571, trifluoroperazine, fluphenazine) affected swelling-induced K⁺ influx in VSMC. In conclusion, K⁺ fluxes triggered in swollen VSMC are mediated by Ba²⁺- and ChTX-sensitive K⁺ channels. These channels are distinct from IK_Ca expressed in erythrocytes. Their molecular origin and systems involved in the swelling-induced Ca²⁺_i-independent signal transduction pathway need further investigation.

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“…33 Red blood cells, although lacking a nucleus, are useful models for membrane transport studies 34,35 and share membrane properties related to VSMC and the endothelium. RBC, which are equipped with IK Ca and inducible nitric oxide synthase, 36,37 respond to K Ca activators producing vasodilatation 7 or to 8Br-cGMP (Delgado et al, 2002, unpublished data) in a manner similar to the VSMC with the activation of K Ca and the efflux of K + .…”

Section: Discussionmentioning

confidence: 99%

Red blood cell K+ could be a marker of K+ changes in other cells involved in blood pressure regulation

Delgado

Delgado-Almeida

2003

J Hum Hypertens

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The aim of this study is to determine whether red blood cell K + content (RBC Ki ) is associated with blood pressure levels and, if so, could RBC Ki be a marker of potassium changes in other cells involved in blood pressure regulation. The study was performed on 50 untreated hypertensives, 32 of their offspring and 50 age-and sex-matched controls. Systolic (SBP) and diastolic (DBP) blood pressures, height, weight, plasma, urine and red blood cell electrolytes were measured in all subjects. RBC Ki was significantly lower in hypertensives than in offspring of hypertensives and normotensive controls. Offspring of hypertensives had significantly lower RBC Ki than normotensive controls. Plasma K + was significantly lower both in hypertensives and offspring of hypertensives when compared to normotensive controls. A significant negative correlation was found in hypertensives between RBC Ki and DBP (r ¼ À0.27, P ¼ 0.04) and in offspring of hypertensives between RBC Ki and DBP (r ¼ À0.43, P ¼ 0.02). A significant correlation was found in hypertensives between RBC Ki and plasma K + (r ¼ 0.3, P ¼ 0.02). A positive correlation with borderline significance was found in hypertensives between RBC Ki and ionized Ca 2+ (r ¼ 0.2, P ¼ 0.1). In conclusion, our results support the hypothesis that RBC Ki is associated with blood pressure levels and that the measurement of RBC Ki levels may represent a biochemical marker for K + changes in other cells involved in blood pressure regulation. Further studies are necessary to explain the exact mechanisms of reduced RBC Ki levels in hypertensive patients and their offspring.

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Na+-H+ exchange and other ion-transport systems in erythrocytes of essential hypertensives and spontaneously hypertensive rats: a comparative analysis

Cited by 58 publications

References 0 publications

Abnormalities of membrane function and lipid metabolism in hypertension A review

Abnormalities of membrane function and lipid metabolism in hypertension A review

Swelling-Induced K<sup>+</sup> Fluxes in Vascular Smooth Muscle Cells are Mediated by Charybdotoxin-Sensitive K<sup>+</sup> Channels

Red blood cell K+ could be a marker of K+ changes in other cells involved in blood pressure regulation

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