Intralymphocytic Sodium in Hypertensive Patients: A Significant Correlation

Ambrosioni, Ettore; Tartagni, F; Montebugnoli, Lucio; Magnani, B

doi:10.1042/cs057325s

Cited by 56 publications

(7 citation statements)

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“…Since 1960 in several studies elevated intracellular Na + levels have been found in red blood cells and in other blood cells from essential hypertensive patients [1,2,4,5,[7][8][9]11]. The overlap between the ranges of hypertensive and normotensive patients, which was often described, may be due to the occurrence of several entities within the unprecisely defined group of essential hypertensives.…”

Section: Introductionmentioning

confidence: 98%

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats

Zidek¹,

Losse²,

Grünwald

et al. 1982

Res. Exp. Med.

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Elevations of intracellular Na+ and Ca2+ in essential hypertension have up to now only been demonstrated in blood cells. Therefore, intracellular Na+ and Ca2+ activities were determined in cultured aortic smooth muscle cells from nine spontaneously hypertensive rats of the Münster strain and from nine normotensive Wistar rats. Intracellular ion activities were determined by ion-selective electrodes. In muscle cells from spontaneously hypertensive rats intracellular Na+ activity was markedly elevated (P less than 0.01), whereas intracellular Ca2+ was not significantly different. This points to the preponderance of genetic causes for the elevation of intracellular Na+, whereas the disturbances in cellular Ca2+ metabolism may additionally require humoral factors to become manifest.

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Section: Introductionmentioning

confidence: 98%

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats

Zidek¹,

Losse²,

Grünwald

et al. 1982

Res. Exp. Med.

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“…The effect of this factor is probably accompanied by an increase in the intracellular concentration of sodium ions in blood cells [3,11], and this increased sodium content may lower the affinity of the [32-adrenoceptors and coupled AC for catecholamine stimulation [8]. Along with this, studies of ouabain suggest that the Na,K-ATPase inhibitor is able to reduce AC sensitivity to sodium ions in a manner which is not yet understood.…”

Section: Resultsmentioning

confidence: 99%

“…Progression of the disease is attended by a decrease in adenylate cyclase (AC) affinity to catecholamines in peripheral blood lymphocytes [8] and a rise in the intracellular concentration of sodium ions in erythrocytes and lymphocytes [3,11]. Interaction of a-and [3-adrenergic receptors with ligands is modulated allosterically by monovalent cations (Na+>Li+>K+), while changes in the receptor affinity to catecholamines correlate with the changes in the intraeellular sodium concentration [10,12,13].…”

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confidence: 99%

Decreased sensitivity of adenylate cyclase to sodium ions in lymphocytes of patients with arterial hypertension

1995

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Patients with arterial hypertension showed decreased sensitivity of isoproterenol-stimulated adenylate cyclase of mononuclear lymphocytes toward sodium ions compared with normotensive donors. Ouabain, an inhibitor of Na, K-ATPase, increased the half-maximal inhibition of adenylate cyclase activity by sodium ions in the cells of healthy subjects and did not change enzyme sensitivity to sodium in the lymphocytes of hypertensive patients.Key Words: sodium; adenylate cyclase; lymphocytes; arterial hypertension; ouabain Changes in the production of different neurotransmitters and hormonal factors, as well as alterations in the cellular mechanisms of hormonal signal transmission via membrane receptors and in the transport of calcium and monovalent cations are typical features of hypertension [4,14]. Progression of the disease is attended by a decrease in adenylate cyclase (AC) affinity to catecholamines in peripheral blood lymphocytes [8] and a rise in the intracellular concentration of sodium ions in erythrocytes and lymphocytes [3,11]. Interaction of a-and [3-adrenergic receptors with ligands is modulated allosterically by monovalent cations (Na+>Li+>K+), while changes in the receptor affinity to catecholamines correlate with the changes in the intraeellular sodium concentration [10,12,13]. Sodium exerts an inhi'bitory effect on AC activity [7]. Data on the phosphorylation of the ct-subunit of Na,K-ATPase by cAMP-dependent protein kinase A and protein kinase C suggest the existence of multiple bonds between the Na,K-ATPase system of active transport of monovalent cations and the cAMP system [6]. Our previous studies demonstrated that the Na,K- ATPase inhibitor ouabain modulates AC activity in the lymphocytes of healthy donors [1] and alters cyclase sensitivity to sodium ions [2]. The purpose of the present study was to investigate the inhibitory effect of sodium on AC activity in the lymphocytes-of patients with arterial hypertension (AH) compared with the cells of normotensive donors. MATERIALS AND METHODSStudies were performed on freshly isolated mononuclear peripheral blood lymphocytes taken from healthy donors and patients with pronounced AH. Cells of 11 normotensive males aged 47+2 years and of 10 males aged 49+3 years with stage IIA of AH according to the classification of Myasnikov (mean arterial pressure 130+3.3 mm Hg) were used in the study. The patients received no medication for 2 weeks prior to the study. For the isolation of lymphocytes blood was taken at 09:00 h from the ulnar vein (from a fasting patient) lying down. The fraction of mononuclear lymphocytes was isolated on a Ficoll-Verographin gradient according to a modified technique [2,5].Basal and isoproterenol-stimulated (100 ~tM) AC activity was determined in lymphocyte homogenates by the method of Salomon [15]

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“…Evidence for the existence of the membrane abnormality in these cells comes mainly from studies of human essential hypertension. Ambrosioni et al 14 have reported an increased lymphocyte sodium content in patients with essential hypertension as compared with that in normotensive controls. Pedersen et al 15 ascribe a higher sodium influx in the lymphocytes from normotensive patients with a family history of hypertension to enhanced sodium-lithium countertransport and unidirectional net sodium flux.…”

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confidence: 99%

Lymphocyte abnormalities in three types of hypertension in the rat.

Furspan¹,

Bohr²

1985

Hypertension

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SUMMARY Lymphocyte number and weight and their sodium and potassium contents and net passive fluxes were measured in spontaneously hypertensive stroke-prone rats, deoxycorticosterone acetate-treated rats, and two-kidney, one clip renal hypertensive rats. Wistar-Kyoto rats were used as controls for the spontaneously hypertensive stroke-prone rats, and normal intact Sprague-Dawley rats were used as controls for the others. Blood lymphocyte count was higher and lymphocyte weight was lower in the hypertensive rats. Intralymphocytic sodium content (millimoles per kilogram of dry weight) was elevated in the three forms of hypertension as compared with control values (spontaneously hypertensive stroke-prone rats, 43.0 ± 1.7 vs Wistar-Kyoto rats, 37.3 ± 1.3; deoxycorticosterone acetate-treated rats, 44.4 ± 3.1 vs Sprague-Dawley rats, 36.1 ± 1.7; one-kidney, one clip rats, 50.5 ± 3.7 vs Sprague-Dawley rats, 38.9 ± 2.0); Intralymphocytic potassium content was not significantly altered in any of the forms of hypertension. Lymphocytes from spontaneously hypertensive strokeprone rats and deoxycorticosterone acetate-treated rats exhibited elevated net sodium fluxes (millimoles per kilogram of dry weight per hour) as compared with those of controls (spontaneously hypertensive stroke-prone rats, 7.00 ± 0.99 vs Wistar-Kyoto rats, 4.89 ± 0.63; deoxycorticosterone acetate-treated rats, 7.58 ± 0.97 vs Sprague-Dawley rats, 5.6 ± 0.64). Net potassium fluxes were significantly elevated only in the spontaneously hypertensive stroke-prone rats (14.07 ± 1.70 vs 8.23 ± 1.04 in Wistar-Kyoto rats). Sodium and potassium fluxes in lymphocytes from two-kidney, one clip rats and Sprague-Dawley rats were not significantly different. The lymphocyte may provide a convenient and suitable system for the study and characterization of a generalized cell membrane abnormality that may be involved in the pathogenesis of hypertension. (Hypertension 7: 860-866, 1985) KEY WORDS • membrane abnormality • sodium flux * potassium flux deoxycorticosterone acetate • renal hypertension • genetic hypertension

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Intralymphocytic Sodium in Hypertensive Patients: A Significant Correlation

Cited by 56 publications

References 1 publication

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats

Intracellular Na+ and Ca2+ activities in aortic smooth muscle cells from spontaneously hypertensive rats

Decreased sensitivity of adenylate cyclase to sodium ions in lymphocytes of patients with arterial hypertension

Lymphocyte abnormalities in three types of hypertension in the rat.

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