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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in intracellular cation metabolism have been implicated in the pathophysiology of essential hypertension. Total magnesium, calcium, sodium and potassium levels were studied in serum erythrocytes and platelets, from 154 subjects (76 hypertensive and 78 normotensives; 104 blacks and 50 whites). In the combined black and white hypertensive group, platelet sodium and calcium and erythrocyte calcium were elevated and serum potassium, serum magnesium and platelet magnesium decreased. In the black hypertensive patients, platelet sodium and calcium and erythrocyte calcium were increased, whereas serum magnesium, serum potassium, platelet magnesium and erythrocyte magnesium were decreased. In the white hypertensive group, platelet sodium and erythrocyte calcium were raised and platelet magnesium was decreased. In the black hypertensive patients, serum and platelet magnesium and serum calcium were negatively and erythrocyte and platelet calcium positively correlated with mean arterial pressure. In the white hypertensive patients platelet sodium was directly related to mean arterial pressure. These results suggest that intracellular sodium and calcium overload and magnesium depletion may be important in the pathophysiology of hypertension. Magnesium disturbances are more consistent and widespread in black hypertensive patients than in white hypertensive patients.
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PMID:Intracellular Mg2+, Ca2+, Na2+ and K+ in platelets and erythrocytes of essential hypertension patients: relation to blood pressure. 142 23

In humans with essential hypertension and in spontaneously hypertensive rats (SHR), insulin resistance may be present even in lean individuals. As the basis for this abnormality is unknown, we have used a newly developed fluorophore to measure intracellular free-Mg2+ concentrations in cultured aortic vascular smooth muscle cells and striated muscle cells from SHR and normotensive Wistar Kyoto (WKY) rats. Intracellular free-Mg2+ levels were lower in both striated muscle cells (SHR, 0.423 +/- 0.077 mmol.L-1 v WKY, 0.559 +/- 0.068 mmol.L-1; P less than .001) and vascular smooth muscle cells (SHR, 0.406 +/- 0.067 mmol.L-1 v WKY, 0.625 +/- 0.077 mmol.L-1; P less than .001) from hypertensive animals. This widespread, intrinsic defect in the regulation of intracellular Mg2+ may explain the increased vascular resistance and reduced insulin sensitivity present in hypertension.
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PMID:Intracellular free-magnesium levels in vascular smooth muscle and striated muscle cells of the spontaneously hypertensive rat. 161 97

The spontaneously hypertensive rats and their genetically matched controls, Wistar-Kyoto, serve as models of essential hypertension. The present study was undertaken to determine whether brush border membrane vesicles obtained from jejunal enterocytes of spontaneously hypertensive rats show increased Na(+)-H+ exchange as part of a generalized membrane disorder. Brush border membrane vesicles were prepared from the jejunum of adult spontaneously hypertensive rats and Wistar-Kyoto rats using an Mg2+/ethylene glycol tetraacetic acid precipitation method. Uptake of 22Na by these vesicles was found to be into an osmotically sensitive intravesicular space rather than mere binding. Initial Na+ uptake by brush border membrane vesicles was greater in spontaneously hypertensive rats than in Wistar-Kyoto rats (P less than 0.05). Higher total and amiloride-sensitive Na+ uptake in spontaneously hypertensive rats occurred in the presence of an outwardly directed pH gradient, and uptake became statistically similar to that of Wistar-Kyoto rats in the absence of a pH gradient. Moreover, amiloride-insensitive Na+ uptake under an outwardly directed pH gradient did not differ significantly between the two groups. The enhanced Na(+)-H+ activity in spontaneously hypertensive rats is not due to altered membrane permeability to protons, as is shown by acridine orange-quenching studies. Kinetic studies for amiloride-sensitive Na+ uptake showed a greater Vmax in spontaneously hypertensive rats compared with Wistar-Kyoto rats (1.46 +/- 0.05 vs. 1.08 +/- 0.08 nmol.mg protein-1.7 s-1) but the Km values were similar in the two groups. These finding, along with similar findings previously reported in vascular smooth muscle and renal tissue of SHR, strongly suggest that an increased Na(+)-H+ exchange is related to the development of hypertension.
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PMID:Increased Na(+)-H+ exchange in jejunal brush border membrane vesicles of spontaneously hypertensive rats. 164 26

An assessment of the ATPase functions of erythrocyte membrane of newly identified subjects having essential hypertension shows that Na+,K(+)-ATPase activity is higher in normal membranes than in membranes of individuals with essential hypertension. A study of the dependence of the enzyme on ATP in the presence of non-limiting concentrations of Na+ (120 mM) and Mg2+ (3 mM) shows that the pump in the membranes of hypertensive individuals, like that of normal humans, is easily saturable by ATP (greater than or equal to 2 microM). Analysis of the results of kinetic studies on the enzyme, in the presence of 5 mM K+, using the Hanes plot, reveals that, although the affinity (Km) of the pump for ATP is unaffected in essential hypertension, its maximum velocity (Vmax) is lower than in normal membranes. Even though the reason for a reduced sodium pump function in essential hypertension is not yet clear, it may not be unconnected with the presence of an endogenous inhibitor or with genetic or diet-induced membrane defects, as previously proposed by other workers in this area of research.
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PMID:Erythrocyte membrane ouabain-sensitive Na+, K(+)-ATPase of hypertensive Nigerians. 165 90

1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl-, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.
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PMID:Plasma and tissue kallikrein-kinin systems during acute administration of frusemide in normotensive and hypertensive humans. 165 30

In the present work we reported the results of the study of erythrocyte membrane Na+,K(+)-adenosine triphosphatase (ATPase) and Mg(2+)-ATPase in patients with essential hypertension and controls. In the 40 patients with hypertension, a more marked decrease of Na+, K(+)-ATPase was observed. The behavior of the enzyme at Mg2+ activation, ouabain inhibition and the response to different temperature suggest the possibility of differences between the two groups. The normal erythrocyte Mg(2+)-ATPase activity in two groups suggest also the possible role of ratio Na+, K(+)-ATPase/Mg(2+)-ATPase in the study of essential hypertension. However the relevance of magnesium and Mg(2+)-ATPase to the pathogenesis of essential hypertension remains unclear but merits further study. On the basis of these considerations the aim of the present study was to identify, in a kinetic approach, the presence of different abnormalities of Na+ transport and Na+, K(+)-ATPase in erythrocytes from patients with essential hypertension. Much evidence has supported the hypothesis that essential hypertension is a heterogeneous disease in the pathophysiological mechanisms as well as in its clinical and therapeutical consideration.
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PMID:[Various properties of the Na+, K(+)-ATPase and the Mg (2+)-ATPase in erythrocytes from normotensive and hypertensive subjects]. 166 78

We have investigated hypertension-associated alterations in intracellular cations in the kidney by measuring intracellular pH, free Mg2+, free Ca2+, and Na+ concentrations in perfused normotensive and hypertensive rat (8-14 weeks old) kidneys using 31P, 19F, and double quantum-filtered (DQ) 23Na NMR. The effects of both anoxia and ischemia on the 23Na DQ signal confirmed its ability to detect changes in intracellular Na+. However, there was a sizable contribution of the extracellular Na+ to the 23Na DQ signal of the kidney. The intracellular free Ca2+ concentration, measured using 19F NMR and 5,5'difluoro-1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid, also increased dramatically during ischemia; the increase could be partly reversed by reperfusion. No significant differences were found between normotensive and hypertensive kidneys in the ATP level, intracellular pH, intracellular free Mg2+, and the 23Na DQ signal or in the extent of the extracellular contribution to the 23Na DQ signal. Oxygen consumption rates were also similar for the normotensive (5.02 +/- 0.46 mumol of O2/min/g) and hypertensive (5.47 +/- 0.42 mumol O2/min/g) rat kidneys. The absence of a significant difference in intracellular pH, Na+ concentration, and oxygen consumption between normotensive and hypertensive rat kidneys suggests that an alteration in the luminal Na+/H+ antiport activity in hypertension is unlikely. However, a highly significant increase (64%, p less than 0.01) in free Ca2+ concentration was found in perfused kidneys from hypertensive rats (557 +/- 48 nM, blood pressure = 199 +/- 5 mmHg, n = 6) compared with normotensive rats (339 +/- 21 nM, blood pressure = 134 +/- 6, n = 4) indicating altered renal calcium homeostasis in essential hypertension. An increase in intracellular free Ca2+ concentration without an accompanying change in the intracellular Na+ suggests, among many possibilities, that the Ca2+/Mg(2+)-ATPase may be inhibited in the hypertensive renal tissue.
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PMID:Multinuclear NMR studies of intracellular cations in perfused hypertensive rat kidney. 174 Apr 16

Essential hypertension is primarily hereditary. The property inherited is present in all cells but because of adaptation and differentiation it is particularly prominent in systemic vascular smooth muscle. This inherited property is manifested functionally as increased reactivity to vasoactive substances, such as (-)noradrenaline and angiotensin II. This abnormal function is present before the onset of hypertension. Vascular hypertrophy and hyperplasia are not only caused by hyperactivity of the smooth muscle and by the hypertension itself but are also trophic effect of the agonists, especially noradrenaline. The only two proteins in vascular smooth muscle which can produce both contractile and trophic effects are the guanosine triphosphate binding protein (Gs) and phospholipase C. Phospholipase C has already been demonstrated to be abnormally active in response to agonists in the spontaneously hypertensive rat and in human essential hypertension. The Gs protein is less likely to be critically abnormal since it is active in the vascular smooth muscle relaxation cascade as well as in contraction. None of the other proteins involved in vascular smooth muscle contraction or relaxation affect both contractile reactivity and cellular growth. There are many secondary effects dependent upon the phospholipase C abnormality such as calcium (Ca2+) cellular content, Ca2+ Mg2+ ATPase pump effects and possibly Ca2+ Na+ exchange. There are also many secondary effects impinging on the phospholipase C abnormality including changes in noradrenaline and angiotensin II metabolism. Present antihypertensive therapy is directed largely at secondary factors dependent upon or influencing the primary phospholipase C cascade. The path is now open for a more direct and basic diagnostic and therapeutic attack.
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PMID:The aetiology of essential hypertension. 177 Apr 74

We have employed 31P nuclear magnetic resonance (NMR) spectroscopy to examine the relationship between cytosolic free Mg2+ ([Mg2+]in), intracellular pH, high energy phosphates, and genetic hypertension using the Wistar-Kyoto rat (WKY) as a control and the spontaneously hypertensive rat (SHR) as a model for essential hypertension. The mean systolic blood pressures (measured using the tail cuff method) of control and hypertensive rats (aged 7 to 12 weeks) were 113 +/- 4 mm Hg (mean +/- 2 SE, n = 14) and 162 +/- 5 mm Hg (mean +/- 2 SE, n = 17), respectively. Intracellular free Mg2+ levels were significantly depleted in the isolated Langendorff perfused hypertensive rat hearts (452 +/- 39 mumol/L, mean +/- 2 SE, n = 17) compared to control hearts (756 +/- 52 mumol/L, n = 14); however, intracellular pH did not differ in the SHR hearts (7.02 +/- 0.03, mean +/- 2 SE, n = 7) compared with controls (7.03 +/- 0.03, n = 7). Although we could not demonstrate a statistically significant difference in the levels of P-creatine or ATP, intracellular Pi was two-fold higher (5.71 +/- 2.28 mmol/L v 2.92 +/- 0.66 mmol/L, n = 4) and the phosphorylation potential, [MgATP]/[MgADP][Pi], was correspondingly lower (3.0 X 10(4) +/- 1.6 x 10(4) v 8.3 X 10(4) +/- 1.4 X 10(4) (mol/L)-1, n = 4) in SHR compared to WKY hearts. These data demonstrate free magnesium depletion in heart muscle and indicate an alteration in cardiac bioenergetics in essential hypertension.
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PMID:Intracellular free magnesium and high energy phosphates in the perfused normotensive and spontaneously hypertensive rat heart. A 31P NMR study. 202 44

We have utilized multinuclear NMR spectroscopy to examine the relationship between cytosolic free Ca2+ ([Ca2+]in), free Mg2+ ([Mg2+]in) and intracellular Na+ ([Na+]in) levels of the intact thoracic aorta and primary hypertension using the Wistar-Kyoto and Sprague-Dawley rats as controls and the spontaneously hypertensive rat as a model for genetic hypertension. Cytosolic free [Ca2+] was measured using 19F NMR of the intracellular Ca2+ indicator 5,5'-difluoro-1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, free [Mg2+] using the 31P resonances of intracellular ATP, and intracellular [Na+] by 23Na NMR in combination with the extracellular shift reagent dysprosium tripolyphosphate. We have found that both the [Na+]in and [Ca2+]in levels were significantly increased in the hypertensive animals relative to normotensive controls (p less than 0.01). Mean systolic blood pressures (using tail cuff method) of control and hypertensive rats were 123 +/- 8 mm Hg (mean +/- 2 S.E., n = 7) and 159 +/- 6 mm Hg (mean +/- 2 S.E., n = 7), respectively. [Na+]in and [Ca2+]in were 21.9 +/- 6.4 mM (mean +/- 2 S.E., n = 7) and 277 +/- 28 nM (mean +/- 2 S.E., n = 5) for the spontaneously hypertensive rats versus 10.1 +/- 1.8 mM (mean +/- 2 S.E., n = 7) and 151 +/- 26 nM (mean +/- 2 S.E., n = 5) for control rats, respectively. A slight difference observed between intracellular free Mg2+ levels in hypertensives (180 +/- 38 microM, mean +/- 2 S.E., n = 4) and controls (246 +/- 76 microM, mean +/- 2 S.E., n = 4) was not statistically significant (p greater than 0.1). These data indicate alterations in the cell membrane ion transport function of the aortic smooth muscle in primary hypertension.
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PMID:NMR measurement of cytosolic free calcium, free magnesium, and intracellular sodium in the aorta of the normal and spontaneously hypertensive rat. 229 35


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