Abnormal sodium efflux in erythrocytes of patients with essential hypertension.

Walter, U.; Distler, A.

doi:10.1161/01.hyp.4.2.205

Cited by 70 publications

(23 citation statements)

References 33 publications

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“…Subsequent reports of erythrocyte cotransport in essential hypertension have usually measured net cation movements, either as net outward Na + and K + losses or as net Rb + uptake, but none of these net movements can give the Vmax and Km of this transport system. 9 ' 12 -l3 In these three studies, as well as in a fourth in which the Na + efflux rate constant alone was measured, 18 the furosemide-sensitive cation movements were uniformly normal in patients with essential hypertension. In contrast, cotransport has been reported to be decreased in hypertensive patients from Paris.…”

Section: Discussionmentioning

confidence: 89%

Erythrocyte cation cotransport and countertransport in essential hypertension.

Wiley¹,

Clarke²,

Bonacquisto³

et al. 1984

Hypertension

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SUMMARY We studied erythrocyte cation cotransport and countertransport systems in 21 and 27 patients with essential hypertension, respectively, all of whom were under 50 years of age, had a diastolic blood pressure level greater than 100 mm Hg, and had a family history of hypertension. The following parameters were normal in nearly all patients: total erythrocyte Na + and K + concentrations, the maximal rate (Vmax) of inward cotransport, the affinity of cotransport with Rb + as the substrate, the net outward cotransport of Na + ions, the passive "leak" influx of Rb, + and the maximal rate of Li + -Na + countertransport. Only four patients gave clearly abnormal results; in two the maximal rate of both cotransport and countertransport was double the normal values, while another two patients demonstrated a greater than twofold increase in passive "leak" influx to Rb + ions. Most of the patients with moderate to severe essential hypertension in this Australian study were characterized by normal erythrocyte cation fluxes, but a few showed elevation of both cotransport and countertransport of cations. (Hypertension 6: 360-368, 1984) KEY WORDS • essential hypertension countertransport erythrocyte cation transport • cotransport F OUR components of Na + transport have been characterized in human erythrocytes, three of which are facilitated by membrane carriers. The first of these three is an active cation pump identified with membrane (Na + + K + )-stimulated adenosine triphosphatase (ATPase) that extrudes Na + from the cell and is inhibited by ouabain.1 The second is a passive cotransport of (Na + + K + ) ions that mediates an equimolar flux of both ions across the membrane by a bidirectional mechanism. This transport system is inhibited by the loop diuretics furosemide and bumetanide.2 The third is Na + -Na + exchange diffusion, which occurs by a mechanism that also mediates the countertransport of Li + for Na + ions. 3 Finally, Na + ions may cross the membrane by a simple passive leak, the magnitude of which is directly proportional to the concentration gradient for this cation. An increase in the maximal rate of Li + -Na + countertransport has been demonstrated in erythrocytes from patients with essential hypertension both in studies

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Section: Discussionmentioning

confidence: 89%

Erythrocyte cation cotransport and countertransport in essential hypertension.

Wiley¹,

Clarke²,

Bonacquisto³

et al. 1984

Hypertension

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“…Supine blood pressure and heart rate were measured after the patient had been resting supine for at least 30 minutes. Venous samples were obtained from the patients at 9 AM after an overnight fast to measure serum sodium, potassium, calcium, magnesium, phosphorus, total cholesterol, triglyceride, and free fatty acid concentrations; plasma renin activity; plasma aldosterone concentration; intraerythrocyte sodium (RBC Na), potassium (RBC K), and magnesium (RBC Mg) 39 with slight modifications. We have described both of these techniques in a previous report.…”

Section: Methodsmentioning

confidence: 99%

Oral magnesium supplementation in patients with essential hypertension.

1989

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To elucidate the effects of magnesium on high blood pressure, a 4-week study of oral magnesium supplementation (MgO 1 g/day) was conducted in 21 outpatients with uncomplicated essential hypertension. During the study, blood pressure and intraerythrocyte sodium concentration decreased significantly, and the erythrocyte ouabain-sensitive Na efflux rate constant (K^ and intraerythrocyte magnesium concentration both increased. Serum triglyceride and free fatty add concentrations were reduced. Furthermore, the elevation in K m significantly and positively correlated with both the increase in intraerythrocyte magnesium concentration and the decrease in mean blood pressure. There was a significant inverse correlation between the prestudy K m and the decrease in mean blood pressure. In addition, when patients were divided according to their overall decrease in mean blood pressure, the prestudy intraerythrocyte sodium concentration was significantly higher in patients with a mean blood pressure decrease of more than 7 mm Hg than that of patients whose mean blood pressure decrease was less than 7 mm Hg. These results suggest that oral magnesium supplementation may lower blood pressure through the activation of a cell membrane sodium pump and may reduce serum lipid concentration. It also suggests that the lower the prestudy K m or the higher the prestudy intraerythrocyte sodium concentration, the more effective the oral magnesium treatment is in lowering blood pressure. Therefore, we concluded that appropriate oral magnesium intake might be effective as a nonpharmacological treatment for essential hypertension. (Hypertension 1989;13:227-232) E pidemiological surveys, clinical investigations, and experimental studies have currently reported '-^ that magnesium may play an important role in the pathogenesis of hypertension and atherogenesis. A recently proposed hypothesis 37 suggests that an impairment of the cell membrane sodium transport system is responsible for the increased total peripheral resistance found in essential hypertension. Magnesium controls cell membrane sodium pump activity, which in turn plays a major role in sodium-potassium transport across cell membranes, thereby affecting vascular tone and reactivity and blood pressure by influencing a Na + -Ca 2+ exchange mechanism. '-8 Furthermore, the atherogenic plasma lipid profile has been improved by magnesium supplementation. -10Thus, this study was designed to evaluate the effects of oral magnesium supplementation on blood pressure and on serum lipid profiles in patients with essential hypertension and to elucidate the From the First Department of Internal Medicine, Kobe University School of Medicine, Kobe, Japan.Address for correspondence: Takaaki Motoyama, MD, First Department of Internal Medicine, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650, Japan.Received August 1, 1987; accepted October 14, 1988. role of magnesium in controlling the cell membrane sodium pump. Patients and MethodsTwenty-one male outpatients with uncomplicate...

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“…Another study, 7 however, detected reduced cotransport in less than half of the pa-tients. Other studies 8 " 10 that used modified methodology to quantitate the furosemide-sensitive erythrocyte cotransport system were unable to detect any abnormality in this transport pathway in Caucasian subjects with essential hypertension. Recently, Adragnaet al" reported elevated erythrocyte Na + ,K + cotransport in Caucasian subjects with essential hypertension and in normotensive offspring with a family history of hypertension.…”

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confidence: 94%

Erythrocyte Na+,K+ cotransport and Na+,K+ pump in black and caucasian hypertensive patients.

Tuck¹,

Gross²,

Maxwell³

et al. 1984

Hypertension

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SUMMARY Alterations in red blood cell (RBC) Na + ,K + pump and in Na + ,K + cotransport (CoT) have been described in essential hypertension (EH). We examined pump and CoT in 50 normotensive (NT) subjects and 58 EH subjects subdivided by race and family history of hypertension (+ FH). RBCs were preloaded with Na + to obtain intracellular levels of 25 mM/liter cells by using the p-chloromercuribenzene sulfonic acid (pCMBS) method. Na + and K + efflux rates into a magnesium-sucrose medium were quantitated in the presence of ouabain and ouabain plus furosemide to define pump and CoT activity respectively. Mean intracellular Na + content was higher (p < 0.05) in black NT and HT subjects compared to Caucasians. Mean RBC CoT was lower in black EH compared to NT and compared to Caucasian NT and HT subjects. Conversely, Caucasian HT patients had higher mean CoT than NT subjects. Subdivision into + FH revealed very little effect of + FH on CoT in black NT and HT subjects. In Caucasian NT and HT subjects with + FH, mean CoT was significantly reduced (<0.3 mM/liter cells/hr) compared to those without + FH. A subgroup of Caucasian EH subjects displayed high CoT (>0.6 mM/liter cells/hr); a + FH had little impact on the high CoT group. There was no correlation between RBC CoT activity and age, sex, severity of hypertension, urinary sodium excretion, and plasma aldosterone. There was a positive correlation (r = +0.47; p < 0.01) between CoT and upright plasma renin activity. In 11 EH patients, reductions in blood pressure by antihypertensive agents did not consistently alter RBC CoT activity. Mean Na + efflux by the RBC Na + ,K + pump measured in washed cells at Vmax was not different in RBCs from black and Caucasian NT and HT subjects. Since CoT function is normally low in RBCs from both black NT and EH subjects, the CoT assay may not be useful as a screening test to identify hypertensive-prone black NT subjects. In Caucasian subjects with a + FH, the assay might have utility as a screening procedure if further evidence links this assay to the pathophysiology of EH. (Hypertension 6: 536-544, 1984)

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Abnormal sodium efflux in erythrocytes of patients with essential hypertension.

Cited by 70 publications

References 33 publications

Erythrocyte cation cotransport and countertransport in essential hypertension.

Erythrocyte cation cotransport and countertransport in essential hypertension.

Oral magnesium supplementation in patients with essential hypertension.

Erythrocyte Na+,K+ cotransport and Na+,K+ pump in black and caucasian hypertensive patients.

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