Intracellular sodium and calcium in essential hypertension

Zidek, Walter; Losse, H; Dorst, K; Zumkley, H; Vetter, Hans

doi:10.1007/bf01728353

Cited by 42 publications

(15 citation statements)

References 9 publications

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“…Altered calcium handling by membranes (reviewed in Reference 3), as well as enhanced intracellular free calcium content, has been reported in various cell types of essentially hypertensive patients and spontaneously hypertensive rats (SHR). 4 " 9 However, the mechanism by which intracellular calcium levels become elevated in cells from hypertensive subjects remains unknown. In these subjects, platelets have been shown to display an increased sensitivity toward a variety of agonists as measured by the cell physiological responses (e.g., shape change, aggregation, release reaction, thromboxane formation).…”

Section: F Ree Cytosolic Calcium Plays An Important Rolementioning

confidence: 99%

Hypersensitivity of phospholipase C in platelets of spontaneously hypertensive rats.

et al. 1987

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SUMMARY Thrombin-induced aggregation and serotonin release were markedly enhanced in platelets from spontaneously hypertensive rats (SHR) when compared with those from normotensive Wistar-Kyoto rats (WKY). Since phosphoinositides are involved in calcium-mediated platelet responses, the metabolism of these lipids was investigated in SHR and WKY by using 32 P-labeled quiescent platelets. In unstimulated cells, both the rate and extent of 32 P incorporation into individual inositol-containing phospholipids and phosphatidic acid were identical in SHR and WKY. This finding suggests that the pool size and basal turnover of phosphoinositides did not differ between the two strains. In contrast, early thrombin-induced phosphoinositide metabolism, when monitored as changes in [32 P]phosphatidic acid, was significantly higher in SHR than in WKY. For example, a 20-second exposure to thrombin, 0.3 U/ml, induced the formation of 1.6 times more [32 P]phosphatidic acid in SHR than in WKY. These results provide evidence for a leftward shift of the dose-response and time-course curves of thrombin-induced [ 32 P]phosphatidic acid formation in SHR. Moreover, the extent of the difference between SHR and WKY was independent of the extracellular calcium concentration. Following thrombin stimulation, [32 P]phosphatidic acid formation likely reflects the initial agonist-receptor interaction; therefore, these results suggest that phospholipase C activity is enhanced in platelets of SHR and that the hypersensitivity of phospholipase C in SHR may play a role in the overall alteration of cell calcium handling and, hence, in the platelet responses of SHR. (Hypertension 10: 497-504, 1987) KEY WORDS • spontaneously hypertensive rats serotonin secretion platelets • phosphoinositides F REE cytosolic calcium plays an important role in the development of tension in vascular smooth muscle, and hence arteriolar resistance, and may be closely related to the development of primary hypertension (see References 1 and 2 for recent reviews). Altered calcium handling by membranes (reviewed in Reference 3), as well as enhanced intracellular free calcium content, has been reported in various cell types of essentially hypertensive patients and spontaneously hypertensive rats (SHR).4 " 9 However, the mechanism by which intracellular calcium levels become elevated in cells from hypertensive subjects remains unknown. In these subjects, platelets

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Section: F Ree Cytosolic Calcium Plays An Important Rolementioning

confidence: 99%

Hypersensitivity of phospholipase C in platelets of spontaneously hypertensive rats.

et al. 1987

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“…11, 20, 88, 89]. Intracellular free Ca2+ concen tration in platelets and red blood cells was found to be elevated in essential hypertensives, although a consider able overlap between values from normotensives and essential hypertensives was observed [8,88,89]. Further more, in normotensives a positive correlation between intracellular free Ca2+ in leukocytes and blood pressure Fig.…”

Section: Essential Hypertensionmentioning

confidence: 99%

“…In red blood cells of normotensive children of hypertensive parents the intracellular Na+ transport, and, to a lesser extent, the intracellular Ca2+ transport is altered [81,88]. Furthermore, the well-known genetic influences in the development of essential hypertension would favor the possibility that also the membrane transport abnormali ties may be genetically determined.…”

Section: Etiologymentioning

confidence: 99%

Calcium and Primary Hypertension

Zidek

Vetter²

1987

Nephron

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The role of dietary calcium in essential hypertension remains controversial. Various studies have found on the one hand a weak negative correlation between blood pressure and Ca²⁺ intake in special groups, and on the other hand a positive correlation between serum Ca²⁺ concentration and blood pressure. Several disturbances of cellular Ca²⁺ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca²⁺ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca²⁺ transport has been proposed as a mechanism. However, disturbances in cellular Ca²⁺ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca²⁺ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still unidentified humoral factor.

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“…[6] Urinary calcium excretion is increased upto a greater extent in hypertensive subjects with higher salt sensitivity index. [7] An increased concentration of serum sodium and decreased concentration of potassium and calcium is seen in essential hypertensive patients. According a study, estrogen is responsible for sodium and water retention by kidneys.…”

Section: Introductionmentioning

confidence: 99%

Studies on Effect of Atenolol and Enalapril on Serum Electrolytes in Pre and Postmenopausal Women with Essential Hypertension

Das¹,

Das²,

Sawalakhe³

et al. 2017

AIMDR

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Background: Essential hypertension is considered one of the major risk factors for morbidity and mortality in modern civilized life. Because of the involvement of ions in contraction of excitable tissues like vascular smooth muscles and myocardium, alteration in the cation transport across cell membrane plays a pivotal role in the pathogenesis of essential hypertension. The aim of this study was to assess the effect of β blocker, atenolol and ACE inhibitor, enalapril on the concentration of serum sodium, potassium and calcium in pre and postmenopausal hypertensive women as compared to normotensive women. Methods: The study was conducted in the medicine department of the institution. For the study, selection of 30 pre and 30 postmenopausal women patients with mild to moderate essential hypertension and 60 normal controls for both the groups was done. The age group of premenopausal hypertensive women was 30-50 years and for postmenopausal hypertensive women it was 50-70 years. Venous blood sample was withdrawn from the study groups and serum was used for estimation of serum sodium, potassium and calcium. 'Systronic' flame photometer was used for estimation of serum sodium and potassium. Results: A significant decrease in the blood pressure of patients treated with both atenolol and enalapril was observed in groups of pre and postmenopausal women with essential hypertension. Significant variations were seen in the concentrations of serum sodium, potassium and calcium (p<0.01) in pre and postmenopausal women with essential hypertension as compared to normal control. We observed significant decrease in the level of serum potassium, calcium and parallel increase in the level of serum sodium in the study subjects before treatment. In postmenopausal essential hypertensive patients, decrease in serum calcium was not found. Conclusion: The effect of β blocker, atenolol on the electrolyte balance shows that it lowers blood pressure by decreasing plasma renin activity. Status of renin in patient may be a marker for the responsiveness to β adrenoreceptor blocker, atenolol. Adenylatecyclase system is also activated in case of atenolol which leads to relaxation.

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Intracellular sodium and calcium in essential hypertension

Cited by 42 publications

References 9 publications

Hypersensitivity of phospholipase C in platelets of spontaneously hypertensive rats.

Hypersensitivity of phospholipase C in platelets of spontaneously hypertensive rats.

Calcium and Primary Hypertension

Studies on Effect of Atenolol and Enalapril on Serum Electrolytes in Pre and Postmenopausal Women with Essential Hypertension

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