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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the binding properties of [3H]ouabain to erythrocytes from normotensive children (n = 83) between the ages of 10 and 18 years (mean resting arterial pressure: 102/57 mm Hg) from normotensive and essential hypertensive parents. Arterial blood pressures of 101/57 and 104/57 mm Hg (subjects with normotensive and hypertensive parents, respectively) were not significantly different between the two groups. Forty-four children had normotensive parents and 39 had hypertensive parents, 51 were white and 32 were black, and 41 were girls and 42 were boys. By using the [3H]ouabain-binding technique, we determined the density of sodium pump sites and the equilibrium dissociation constants in erythrocytes from these children. Possible effects of race, sex, or parental hypertension status on pump sites and dissociation constants were tested with a three-way analysis of variance (ANOVA). Race had a major effect on the dissociation constant: blacks had a significantly higher value than did whites (p = 0.002). We also found a race by sex by parental hypertension status interaction (p = 0.04) with black girls with hypertensive parents having the highest value. There was no effect of race, sex, or status on sodium pump site density. Age, height, weight, resting arterial blood pressure, and plasma Na+ and K+ concentrations did not correlate with the dissociation constants. These data suggest that, among the groups we studied, black girls with hypertensive parents had erythrocytes with the lowest binding affinity for ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Race, sex, and family history of hypertension and erythrocyte sodium pump [3H]ouabain binding. 215 3

Many membrane abnormalities have been described in human essential hypertension that may lead to an increased intracellular Na+ content, an example being reduced Na+ efflux by the sodium pump. We have previously found increased Na(+)-H+ antiport activity in leucocytes of hypertensive subjects. In the present study we examined the kinetics of this pump in 16 hypertensive and 20 carefully matched normotensive subjects by loading cells to different intracellular pH levels (as measured by fluorimetry) using a double-ionophore technique. The maximal rate of ethyl isopropyl amiloride-sensitive H+ efflux was significantly raised in leucocytes from the hypertensive subjects [75.3 +/- 6.2 versus 48.8 +/- 2.1 mmol/l per min in normotensives (mean +/- s.e.m.); P less than 0.001]. There was no difference in the affinity of the Na(+)-H+ antiport for intracellular H+. Intracellular buffering power at different internal pH levels in the range 6.0-7.1 did not differ in the two groups. We conclude that one reason for the reported intracellular alkalinity and increased sodium content of leucocytes from hypertensive subjects in bicarbonate-free media could be an increased number of active Na(+)-H+ exchangers or an increased turnover rate for each exchanger. A similar defect in vascular smooth muscle could account for the increased tone and thickening of the media. The abnormal maximal transport capacity of the leucocyte may be a useful membrane marker for future studies in human hypertension.
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PMID:Kinetics of the human leucocyte Na(+)-H+ antiport in essential hypertension. 216 87

Pregnancy-induced hypertension may be linked with sodium pump inhibition and an increase in vascular myocytic tone and, hence, flow impedance. All of the findings of studies on circulating plasma and blood cells are not, however, consistent with this hypothesis. We therefore assessed sodium pump numbers and cation transport in lymphocytes from 23 women with untreated pregnancy-induced hypertension, 28 normotensive pregnant women and 28 healthy non-pregnant women. We measured the maximum 3H-ouabain binding capacity to determine the sodium pump activity and the apparent dissociation constant (the reciprocal of which estimates binding affinity) by Scatchard analysis, ouabain-sensitive (pump-mediated) 86rubidium influx and ouabain-resistant (pump-independent) influx in lymphocytes in vitro. Pregnant women, whether normotensive or hypertensive, had significantly more sodium pump activity and a higher pump-mediated and pump-independent 86rubidium influx than non-pregnant women. Sodium pump activity and the pump-mediated and pump-independent 86rubidium influx all reached normal, non-pregnant levels in normotensive pregnant women 6 weeks after delivery, but remained high in women with pregnancy-induced hypertension. The normotensive and hypertensive pregnant women and non-pregnant women all had similar ouabain binding affinity. The results of our study do not support the circulating sodium pump inhibitor hypothesis in pregnancy-induced hypertension.
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PMID:Sodium pump numbers and cation transport of lymphocytes in pregnancy-induced hypertension. 217 75

Hypertension and diabetes mellitus are chronic medical conditions that frequently coexist. In the United States, it is estimated that 10 million persons suffer from diabetes mellitus, 60 million from hypertension, and 3 million from the combination of the two. There may be a causal relationship between hypertension and diabetes. Obesity may be a precipitating factor for both hypertension and non-insulin-dependent diabetes mellitus. Those with insulin-dependent diabetes mellitus generally become hypertensive only with the onset of nephropathy. Glucose tolerance, insulin resistance, and hyperinsulinemia frequently occur with essential hypertension and may be aggravated by hypertension therapy, especially with diuretics and beta-blockers. Hyperinsulinemia may be an important common factor promoting sodium retention, sympathetic nervous system stimulation, and inhibition of the sodium pump. The Working Group on Hypertension in Diabetes has outlined a flexible modified version of the stepped-care approach to the treatment of hypertension in diabetes. Management is complex because diabetes is associated with autonomic neuropathy, sexual dysfunction, hyperlipidemia, and fluid and electrolyte disorders. All these problems can be exacerbated by antihypertensive treatment. Nonpharmacologic measures, which address weight reduction and sodium restriction, are logical, but aggressive antihypertensive medication is invariably necessary. Diuretics and/or beta-blockers were the mainstay of treatment until the introduction of angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers. These newer agents have no deleterious effects on carbohydrate metabolism and are generally better tolerated. Antihypertensive therapy may slow the rate of deterioration in diabetic nephropathy. This was first shown with diuretics, beta-blockers, and hydralazine and more recently with ACE inhibitors, which provide effective blood pressure control and a significant drop in albuminuria without affecting the glomerular filtration rate adversely. ACE inhibition may also lead to increased insulin sensitivity and glucose disposal rate. Long-term trials are needed to assess the effects of these new agents on the treatment of hypertension in the diabetic population.
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PMID:Diabetes mellitus and hypertension. 222 Jul 97

Endogenous factors cross-reacting with antidigoxin antibodies have been found in several tissues and body fluids of animals and humans, using commercially available digoxin radioimmunoassay or enzyme immunoassay methods. The chemical characteristics of these endogenous factors are, at present, unknown, although it has been suggested that they could be substances with low molecular weight. Experimental studies and theoretical considerations indicate that endogenous digitalis-like factors (DDLFs), in addition to the ability to react with antibodies, might also bind to the specific cellular receptor of the cardiac glycosides and thus inhibit the membrane Na+/K(+)-ATPase (sodium pump). Therefore, EDLF can be an endogenous modulator of the membrane sodium-potassium pump and several authors have suggested that EDLF could play a role in the regulation of fluids and electrolytes, muscular tone of myocardial and also in the pathogenesis of arterial hypertension. In this review, the authors discuss the hypothesis that, in metabolic diseases such as diabetes mellitus, obesity and acromegaly, the sodium retention and volume expansion, possibly due to exaggerated sodium intake, and/or exogenously induced peripheral hyperinsulinemia and high levels of growth hormone, could trigger a sustained release of EDLF, which in turn increases the blood pressure.
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PMID:Is the endogenous digitalis-like factor the link between hypertension and metabolic disorders as diabetes mellitus, obesity and acromegaly? 222 23

The purpose of the study was to determine the effect of dietary calcium intake on blood pressure and sodium ion transport of red blood cells (RBC) in spontaneously hypertensive rats (SHR). The SHR were fed by diet with three different levels of calcium contents as follows; 0.1% of Ca (low Ca diet), 0.6% of Ca (normal Ca diet) and 4.0% of Ca (high Ca diet) between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte sodium efflux, as well as sodium and potassium contents in the RBC were measured. On the low calcium diet, SHR showed an enhancement of hypertension. On the high calcium diet, SHR showed an attenuation of the increase in blood pressure. In proportion to the levels of dietary calcium contents, SHR had a lower level of sodium contents in the RBC and a higher activity of the sodium pump. The passive sodium permeability and sodium-potassium cotransport in SHR were similar among low, normal and high calcium diet groups. It is concluded that the amounts of dietary calcium might be related to the regulation of blood pressure by changing the sodium pump of the cell membrane in SHR.
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PMID:[Effect of dietary calcium on erythrocyte sodium pump in spontaneously hypertensive rats (SHR)]. 234 73

To test whether leucocyte sodium pumps function abnormally in patients with essential hypertension specific tritium-ouabain binding (number of pumps) and ouabain sensitive uptake of rubidium-86 (86Rb+) (transport activity) were measured in mononuclear leucocytes from 37 untreated hypertensive patients and 85 normotensive subjects. Ouabain binding was lower and transport activity per binding site higher in the hypertensive patients before incubation (p less than 0.001), but both variables were normal after incubation for 72 hours with fetal calf serum. To determine whether a circulating inhibitor of sodium pumps was present in patients with hypertension ouabain binding and 86Rb+ uptake were measured in normal leucocytes before and after incubation for 72 hours with serum from 13 untreated hypertensive patients and 18 normotensive subjects. Ouabain binding was lower after incubation of cells with serum from hypertensive patients than after incubation with normal serum both before (p less than 0.01) and after (p less than 0.001) dialysis of the serum. The results suggest that in hypertension a circulating serum inhibitor of the sodium pump causes a chronic but reversible reduction in the number of pumps.
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PMID:Reversible inhibition of leucocyte sodium pumps by a circulating serum factor in essential hypertension. 242 43

In this article, we review the data about Na+ and K+ lymphocyte content in young subjects with borderline hypertension. These data indicate that many borderline subjects have an abnormally high lymphocyte Na+ content (Nai) and that their pressor response to stress and exercise is directly related to Nai. Lymphocyte K+ content (Ki) is increased in about 50% of borderline subjects. Subjects in whom Ki is high, in comparison with those having a normal Ki, have a lower Nai and lower diastolic blood pressure. This suggests that these subjects have an activation of some compensatory mechanism, possibly an increase in sodium pump function. A humoral factor causing an increase in Nai was detected not only in the plasma from essential hypertensives, but also in the plasma from borderline subjects and from normal subjects with familial hypertension having high Nai. This indirect evidence of a plasma factor impairing Na+ transport was confirmed by direct measurements of the plasma ability to inhibit Na+/K+ adenosine triphosphate. Moderate short-term dietary salt restriction reduces Nai and, proportionally, pressor response to stress. In the long-term, resting blood pressure is also reduced. Dietary K+ supplementation reduces pressor response to handgrip but not resting blood pressure. Intralymphocytic Na+ content is a good predictor of future sustained hypertension, since subjects with normal Nai do not develop hypertension within 5 years, whereas subjects with high Nai develop hypertension in 31% of cases. These subjects also have an altered pressor response to mental stress and do not respond to the low-salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular and humoral factors in borderline hypertension. 242 78

The possible roles of a humoral sodium pump inhibitor and atrial natriuretic peptide in low renin hypertension are considered, relying heavily on data from a classical animal model of low renin hypertension, the reduced renal mass-saline model in the rat, and on data uncovered by a new literature survey of the two agents in various normotensive and hypertensive states. Based on these data, particularly those indicating both agents are released by volume expansion, our current view is that low renin hypertension is in part generated by the sodium pump inhibitor and is in part moderated by atrial natriuretic peptide. We suggest that the atrial natriuretic peptide compensates for increased volume due to reduced renal function and/or increased salt intake and that in low renin hypertension the compensation is not sufficient to return volume and pressure to normal. In this view, the sodium pump inhibitor is prohypertensive, via actions on blood vessels and heart, and atrial natriuretic peptide is antihypertensive, via actions on kidney and the cardiovascular system.
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PMID:Natriuretic hormones in low renin hypertension. 243 43

The possible role of endogenous sodium pump inhibitors was studied in salt-sensitive rats of Dahl strain which were influenced by high salt intake either in youth (from prepuberty) or only in adulthood. The aim of our study was to search for the relations between the age-dependent blood pressure response to high salt intake and the changes in volume or distribution of body fluids, red cell ion transport or Na+,K+-ATPase activity in various tissues of salt-sensitive (S/JR) and salt-resistant (R/JR) rats. Salt hypertension was especially pronounced in those S/JR rats which were maintained on a high-salt diet from prepuberty. This was accompanied by the moderate expansion of body fluids in young but not in adult hypertensive animals. Na+,K+-ATPase activity was suppressed in both kidney and heart of young S/JR rats with salt hypertension while this was not true in adult hypertensive animals. On the other hand, no inhibition of sodium pump was observed in brain microsomes and erythrocytes of severely hypertensive young S/JR rats. Moreover, no increased levels of endogenous sodium pump inhibitors were detected in plasma of salt hypertensive S/JR rats. Thus our study indicated the age-dependent suppression of sodium pump activity in some tissues of salt hypertensive Dahl rats but we failed to confirm increased levels of circulating sodium pump inhibitors in young salt hypertensive rats.
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PMID:Sodium pump activity in young and adult salt hypertensive Dahl rats. 243 46


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