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

A wide range of abnormalities of membrane sodium and potassium transport can be demonstrated in patients with essential hypertension, and in rats with genetic hypertension and with some forms of experimental hypertension. In the human red cell increased permeability to sodium and potassium, increased ouabain-sensitive sodium pumping, lithium-sodium counter-transport, and frusemide-sensitive co-transport have been described; by contrast, in the human leucocyte sodium pumping is reduced. In the spontaneously hypertensive rat and the rat with mineralocorticoid-induced hypertension, increased permeability to sodium and potassium, with increased ouabain-sensitive pumping, is shared by the red cell and the arterial smooth muscle. This abnormality is associated with decreased cell-membrane affinity for calcium and increased cell-membrane viscosity. It is proposed that in essential hypertension the decreased membrane affinity for calcium is a primary pathogenetic change giving rise to secondary changes in sodium and potassium transport.
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PMID:Ion transport in hypertension. 676 31

86Rubidium influx and Na--K-cotransport have been investigated in erythrocytes of mild essential hypertensives and normotensives devoid of familial hypertension. For measurement of cotransport Na-loaded/K-depleted erythrocytes were used while rubidium influx (with and without ouabain) was determined under physiological conditions. Both transport systems were linear in time, the interassay variances in a range of about 10%. The patients with essential hypertension exhibited a decreased rubidium influx compared to the normotensive controls. Ouabain-sensitive fluxes were not significantly different between the two groups, whereas ouabain-resistent rubidium influx was diminished in the group of the patients. Na--K-cotransport was also found to be decreased in essential hypertension. There was no correlation between cotransport and Rb-influx. The results indicate changes in cation fluxes in erythrocytes of essential hypertensives, the Na--K-cotransport being rather more altered than rubidium influx. It is speculated that hypertensive persons with reduced rubidium flux rates may represent a subpopulation of essential hypertension and that their high blood pressure may be additionally influenced by exogeneous factors e.g. enhanced sodium uptake.
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PMID:[Cation flux in erythrocytes of patients with essential hypertension]. 687 84

Sodium and potassium ion transport systems were studied in erythrocytes from spontaneously hypertensive Okamoto rats (SHR), hypertension-prone Sabra rats (SbH), and one-kidney one-clip Goldblatt hypertensive rats, and compared with Wistar-Kyoto normotensive rats (WKY), hypertension-resistant Sabra rats (SbN), and sham-operated Wistar rats. We observed the following: (1) An increased net potassium influx and a reduced net sodium extrusion occurred in SHR. The increased potassium influx was inhibited by ouabain, indicating an increased sodium ion pump activity. Bumetanide-sensitive sodium extrusion was lower in SHR than it was in WKY, indicating abnormally low outward sodium-potassium cotransport fluxes. (2) Passive sodium ion permeability was increased in SbH compared with SbN. Cotransport was normal in SbH rats. (3) Sodium-potassium cotransport and passive permeability were normal in renovascular hypertension. (4) After a chronic or acute sodium load, the sodium content increased in erythrocytes from SHR and SbH but not in those of normotensive or renal hypertensive rats. It appears therefore that erythrocyte membrane abnormalities leading to an increased intracellular sodium concentration are only present in genetic hypertension. The reduction of outward sodium-potassium cotransport observed in SHR is identical to that previously reported in human essential hypertension, suggesting that it may be considered as a genetic marker.
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PMID:Erythrocytic sodium ion transport systems in primary and secondary hypertension of the rat. 695 75

Transport features of calcium in red cells of rats with spontaneous genetic hypertension (SHR) have been studied. It is shown that in the presence of calmodulin the rate of calcium accumulation by the inside-out vesicles of SHR red cell membranes is roughly twice less than in the control normotensive rats. It is suggested that upset interrelationship between calmodulin and Mg-Ca-ATPase of plasma membrane may be the cause of increase of intracellular calcium recorded in a number of tissues in primary hypertension.
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PMID:[Calcium transport in the erythrocytes of rats with spontaneous hypertension: characteristics of the effect of calmodulin]. 710 56

1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.
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PMID:Aggravation of hypertension in spontaneously hypertensive rats by Heymann nephritis. 723 40

1. The sodium concentration in lymphocytes was measured in a group of 66 normotensive subjects (40 without familial hypertension and 26 with familial hypertension), in a group of 81 patients with essential hypertension and in a group of 14 patients with secondary hypertension. 2. The mean value (+/- SD) in normotensive subjects with no history of familial hypertension was 21.9 +/- 3.1 mmol/kg wet weight, which was significantly lower (P less than 0.005) than that of normotensive subjects with familial hypertension (mean value 27.9 +/- 4.2 mmol/kg). Lymphocyte sodium concentration was significantly higher in patients with essential hypertension (33.2 +/- 3.3 mmol/kg; P less than 0.001) than in the subjects with normal blood pressure without familial hypertension. 3. In the patients with essential hypertension there was a significant correlation between lymphocyte sodium concentration and systolic (P less than 0.005), diastolic (P less than 0.001) and mean (P less than 0.001) blood pressure. In the normotensive subjects there was no correlation between the lymphocyte sodium concentration and the blood pressure. 4. The patients with secondary forms of hypertension had normal lymphocyte sodium concentration, except in the case of Conn's disease. 5. Incubation with ouabain increased lymphocyte sodium concentration in the normotensive subjects and patients with essential hypertension; the final sodium concentration was similar in the two groups. 6. When lymphocytes from normotensive subjects without familial hypertension were incubated in plasma of patients with essential hypertension there was an increase in their sodium content.
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PMID:Increased intralymphocytic sodium content in essential hypertension: an index of impaired Na+ cellular metabolism. 726 42

Several abnormalities concerning sodium (Na+) transport in erythrocytes of essential hypertensive patients have been recently observed. An abnormal extrusion of an erythrocyte Na+ load was described in our laboratory. This defect appeared to be specific for essential hypertension since it was absent in the secondary forms of the disease. The present investigation was performed on 194 Caucasian subjects with essential hypertension or born of hypertensive parents, 86 normotensive controls, and 14 families (78 subjects) studied over two to three generations. The distribution pattern of the erythrocyte defect is compatible with the expression of a single gene transmitted according to an autosomic and dominant mode. To confirm the genetic association between the red blood cell abnormality and primary hypertension, genetically hypertensive rats were investigated in parallel to our clinical studies. A reduction in the net Na+ extrusion from red blood cells was found in two varieties of genetic hypertension (SHR and H-prone-Na+-sensitive Sabra rats). The abnormality could be detected before the development of a significant hypertension. When these various rat sub-strains were acutely or chronically loaded with Na+ (either intraperitoneally or orally), a significant increase in erythrocyte Na+ content was observed only in those substrains having a genetic propensity to develop hypertension. This finding, which appears to be a consequence of the reduction in net Na+ efflux, is of interest for several reasons. It confirms the existence of a close association between a genetic predisposition to develop high blood pressure and cell Na+ retention in the presence of an excess Na+ intake. It draws attention to the possible role of intracellular Na+ in the pathogenesis of primary hypertension. Of more practical importance, the abnormal Na+ handling in erythrocytes may be a genetic marker of primary hypertension.
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PMID:Abnormal erythrocyte cation transport in primary hypertension. Clinical and experimental studies. 726 80

Multiple heritable traits are associated with essential (genetic) hypertension in humans. Because chromogranin A is increased in both human and rodent genetic hypertension, we examined the influence of heredity and blood pressure on chromogranin A in humans. In estimates derived from among- and within-pair variance in monozygotic versus dizygotic twins, plasma chromogranin A displayed significant (F15,18 = 2.93, P = .016) genetic variance (sigma 2 g), and its broad-sense heritability was high (h2B = 0.983). Plasma chromogranin A was increased in essential hypertension (99.9 +/- 6.7 versus 62.8 +/- 4.7 ng/mL, P < .001) but was influenced little by genetic risk for (family history of) hypertension (in normotensive or hypertensive subjects), by race, or by several antihypertensive therapies (angiotensin-converting enzyme inhibitor, diuretic, or beta-adrenergic antagonist). In normotensive subjects at genetic risk for essential hypertension, neither basal nor sympathoadrenal stress-evoked chromogranin A differed from values found in subjects not at risk. In established essential hypertension, plasma chromogranin A responses to adrenal medullary (insulin-evoked hypoglycemia) or sympathetic neuronal (dynamic exercise) activation were exaggerated, whereas responses to sympathoadrenal suppression (ganglionic blockade) were diminished, suggesting increased vesicular stores of chromogranin A and an adrenergic origin of the augmented chromogranin A expression in this disorder. We conclude that plasma chromogranin A displays substantial heritability and is increased in established essential hypertension. Its elevation in established hypertension is associated with evidence of increased vesicular stores of the protein and with adrenergic hyperactivity but is influenced little by customary antihypertensive therapies. However, the chromogranin A elevation is not evident early in the course of genetic hypertension.
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PMID:Chromogranin A in human hypertension. Influence of heredity. 760 27

1. We have recently identified a candidate gene for rat genetic hypertension, termed SA, by identifying an mRNA species that shows markedly higher expression in the kidneys of spontaneously hypertensive rats (SHR) than in those of Wistar-Kyoto rats (WKY). 2. Subsequent genetic co-segregation analyses by ourselves and others indicated that the SA gene locus did indeed influence blood pressure. Moreover, in a preliminary association study, we found an association of a polymorphism of the human SA gene with essential hypertension. 3. Further studies to identify functions of the SA gene products are required before reaching a definite conclusion.
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PMID:Molecular genetics of the SA gene. 788 84

We have recently identified a candidate gene for rat genetic hypertension by identifying an mRNA species that shows markedly higher expression in the kidneys of spontaneously hypertensive rats than in those of Wistar-Kyoto rats. By using a restriction fragment length polymorphism, we carried out cosegregation analyses between the genotype of the SA gene and blood pressure in three F2 cohorts and observed significant effects of the SA gene on blood pressure in all of those cohorts. In the present study, we have isolated a human counterpart of the rat SA gene to investigate the possible association between the human SA gene and human essential hypertension. The deduced amino acid sequence from the isolated human SA cDNA consisted of 578 amino acid residues and had slight homology to a bacterial enzyme, acetyl-coenzyme A synthase. The human gene was mapped to the human chromosome 16 with the use of a rodent/human somatic hybrid cell panel. A restriction fragment length polymorphism was found with the restriction enzyme Pst I, and the allele frequencies were compared between hypertensive and control groups. The hypertensive group consisted of 89 individuals, and the Pst I rare allele (A2 allele) frequency in this group was 0.270. The control group consisted of 81 healthy normotensive individuals whose precise clinical data were available; the A2 allele frequency in this group was 0.09. Significant differences in the frequency of the A2 allele were observed between the hypertensive and control groups (P = .0001). The present findings provide favorable evidence that the SA gene is a candidate gene for human essential hypertension and also provide a starting point for future studies.
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PMID:Human SA gene locus as a candidate locus for essential hypertension. 790 20


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