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

In search for a diagnostic marker for essential hypertension, we investigated the activity of the ouabain sensitive Na-K-ATPase and the ouabain insensitive ATPase in erythrocyte ghosts of 57 patients with essential hypertension, 12 patients with renal hypertension, 6 patients with Cushing's syndrome and 4 patients with primary hyperaldosteronism. Na-K-ATPase-activity was increased in patients with essential hypertension and in patients with renal hypertension compared with controls with a considerable overlap. Na-K-ATPase-activity was increased in all patients with Cushing's syndrome but was not different from the control group in patients with Conn's syndrome. Ouabain-insensitive ATPase-activity was similar in all patients and in normotensive controls. The serum of patients with essential hypertension did not exhibit an ouabain-like ATPase-inhibiting activity when incubated with erythrocyte ghosts of normotensive controls. In our hands, determination of the Na-K-ATPase-activity in erythrocyte ghosts cannot be used as a diagnostic marker for essential hypertension.
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PMID:Na-K-ATPase in erythrocyte ghosts is not a marker for primary hypertension. 627 8

Various parameters of erythrocyte membrane sodium transport were measured in patients with untreated essential hypertension, in the normotensive offspring of parents with hypertension, and in patients whose hypertension had been controlled by medication. Net sodium efflux, measured by an isotopic tracer technique, was 2.12 +/- 0.17 mM Na+/1 of red blood cells (RBCs)/hr in patients with untreated essential hypertension, compared with 1.55 +/- 0.12 mM Na/1 of RBCs/hr in a group of normotensive controls (p less than .025). Partitioning sodium efflux into ouabain-sensitive and ouabain-insensitive components revealed a significant elevation of both components of membrane sodium transport in the patients with untreated essential hypertension. Ouabain-sensitive sodium efflux was 1.38 +/- 0.09 mM Na/1 RBCs/hr in the patients, compared with 1.04 +/- 0.07 mM Na/1 RBCs/hr in the controls. Ouabain-insensitive sodium efflux was also increased from 0.51 +/- 0.05 mM Na/1 RBCs/hr in the controls to 0.74 +/- 0.09 mM Na/1 RBCs/hr in those with untreated hypertension. Despite these changes in sodium efflux, Na,K-ATPase activity in the erythrocyte membrane, measured at maximum velocity (Vmax), was normal, suggesting that the observed abnormalities in membrane sodium transport in patients with untreated essential hypertension resulted from a change in pump control mechanisms rather than a change in enzyme activity. With the techniques used in this study we were unable to identify changes in erythrocyte membrane transport in the normotensive offspring of hypertensive parents. Membrane sodium transport was also examined in hypertensive patients whose blood pressure had been controlled by medication. In this group it was found that erythrocyte sodium transport did not differ from that in our control group, which suggests that treatment of hypertension can modify fundamental pathophysiologic changes at the level of the cell membrane.
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PMID:Erythrocyte membrane sodium transport in patients with treated and untreated essential hypertension. 630 25

Red cell sodium and potassium concentrations, and total ouabain-sensitive and ouabain-insensitive first order red constants for sodium efflux, were measured in 15 patients (11 female, 4 male) with essential hypertension (162 +/- 14/99 +/- 7 (s.d. mmHg) and 15 normotensive control subjects (117 +/- 17/64 +/- 10 mmHg) individually matched for age (45.8 +/- 10 versus 45.7 +/- 10 years, respectively, sex, weight (68.6 +/- 16.1 versus 64.7 +/- 11.2 kg) and blood group. To test for possible plasma inhibitors of sodium transport in hypertension, total efflux rate constants were measured in red cells incubated in two plasma samples, from either the same or the complementary (paired) subjects, respectively. Intracellular sodium was significantly increased in patients (11.8 +/- 3.45 versus 8.75 +/- 2.48 mmols/l of red cell water; P = 0.023). Intracellular potassium and total and ouabain-sensitive sodium efflux rate constants, were similar in both groups. Sodium efflux was similar when cells were incubated in the homologous and complementary plasma samples. Ouabain-insensitive rate constants were decreased in the patients (0.16 +/- 0.08 versus 0.20 +/- 0.05 h-1) but the difference was of borderline significance (P = 0.059). These results confirm the presence of abnormal intracellular sodium concentrations and membrane transport in essential hypertension but are not consistent with the suggestion that the abnormalities are due to a circulating sodium transport inhibitor.
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PMID:Evidence against a circulating ouabain-like transport inhibitor as a cause of increased red cell sodium in essential hypertension. 659 99

The effect of local infusion of ouabain into the forearm vascular bed has been examined in 15 normotensive male volunteers in an attempt to define the nature of the functional abnormalities of the resistance vessels in primary hypertension. Ouabain and other drugs were infused into the brachial artery and forearm blood flow was measured by venous occlusion plethysmography. Infusion of ouabain at 2 micrograms/min for 1 h caused a 26% reduction in forearm blood flow with a small rise in systemic arterial pressure; the increase in vascular resistance was unaffected by prior treatment with phentolamine. After infusion of ouabain the dilator response to potassium was reduced by 33% but the responses to verapamil and sodium nitroprusside were unchanged. The results show that acute depression of sodium pump activity by ouabain reproduces the increased resting resistance and impaired response to potassium that are seen in hypertension. It does not reproduce the relative enhancement of responsiveness to verapamil that is also observed in the resistance vessels of patients with hypertension and this abnormality must have some other cause.
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PMID:Effect of local infusion of ouabain on human forearm vascular resistance and on response to potassium, verapamil and sodium nitroprusside. 668 Oct 36

1. The dependency of arteriolar tone on the activity of the Na+ -K+-pump was studied in 17 normotensive (NT) males, aged 20-71 yr, without heredity for essential hypertension and 28 male patients with essential hypertension, aged 18-63 yr, by measuring forearm blood flow response to intra-arterial infusion of the Na+-K+-pump inhibitor ouabain. 14 of the patients were classified as borderline essential hypertensives (BHT) and 14 as established essential hypertensives (EHT). 2. Ouabain in incremental dosages 0.4-16 micrograms/100 ml tissue induced a vasoconstrictive response in the forearm with a maximal effect to 8 micrograms/100 ml tissue, which was not associated with an increase in regional noradrenaline release. 3. The vasoconstriction to ouabain 8 micrograms/100 ml was 29.6 +/- 6.8% in NT (P less than 0.001); 51.9 +/- 8.4% in BHT (P less than 0.001) and 36.0 +/- 12.7% in EHT (P less than 0.05). This response was greater in BHT than in NT (P less than 0.05) but not different in NT and EHT and did not correlate with age either in NT or in BHT and EHT taken together. 4. Our findings suggest an increased activity of the arteriolar Na+ -K+-pump in the early phase of essential hypertension which may to some extent correct a raised intracellular Na+; the latter being the consequence of an increased passive permeability to Na+. The activity of the arteriolar Na+ -K+-pump appears to be decreased in the later as compared to the early phase of essential hypertension.
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PMID:Inhibition of the arteriolar smooth muscle NA+ -K+-pump induces an enhanced vasoconstriction in borderline but not in established essential hypertension. 682 33

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

We investigated both sodium-lithium countertransport (Na-Li CT) and ouabain-sensitive sodium transport (Na pump) of erythrocytes in healthy subjects (group A), patients with non-insulin-dependent diabetes (NIDDM) without nephropathy (group B), patients in the proteinuric stage (group C), and those in the renal insufficiency stage (group D). Erythrocytes from all four groups had a similar initial water and ionic content and were loaded with similar degrees of Li and Na for efflux studies. There were no significant differences in erythrocyte Na-Li CT or Na pump among the four groups. However, the maximal rate of Na-Li CT was significantly higher in a group of subjects with essential hypertension when compared with groups A, B and C, consistent with the view that there is a genetic marker for essential hypertension. Ouabain-insensitive Na efflux (Na leak) of erythrocytes was found to be significantly higher in group D than in groups A or B. Also, a significant positive correlation existed between Na leak and urine protein levels of the subjects studied. Our results thus indicate that in contrast with insulin-dependent diabetic patients (IDDM) where an elevated Na-Li CT is observed, with diabetic nephropathy, Na-Li CT in NIDDM is apparently not associated with nephropathy; rather the ouabain-insensitive Na efflux appears to be correlated with the stages of nephropathy in NIDDM. The association suggests that the rate of ouabain-insensitive Na efflux may provide an index for assessing the degree of nephropathy in NIDDM patients.
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PMID:Abnormalities of sodium transport in non-insulin-dependent diabetes: association with renal disease. 810 99

The purpose of the present study was to examine alterations in membrane fluidity of erythrocytes in essential hypertension by means of an electron paramagnetic resonance (EPR) and a spin labeling method. In addition, we investigated the effects of ouabain on the fluidity of erythrocytes, and elucidated a possible role of Na+, K(+)-ATPase in the regulation of membrane fluidity in hypertension. Erythrocytes obtained from patients with essential hypertension were examined compared with those from age-matched normotensive subjects. The EPR spectra for 5-nitroxide stearate incorporated into erythrocyte membranes were studied. The values of the outer hyperfine splitting and order parameter (S) of the EPR spectra were significantly higher in patients with essential hypertension than in normotensive subjects. This finding shows that the membrane fluidity of erythrocytes might be lower in essential hypertension. Ouabain-loading of erythrocytes decreased the membrane fluidity (S value was increased). The ouabain-induced changes were significantly greater in essential hypertension than in normotensive subjects. These results demonstrate that the membrane fluidity of erythrocytes might be lower in essential hypertension than in normotensive subjects. Furthermore, the membrane fluidity might be highly dependent on the Na+, K(+)-ATPase activity in essential hypertension, which would suggest an abnormality in Na(+)-related cellular functions in hypertension.
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PMID:Membrane fluidity of erythrocytes and its modulation by ouabain in essential hypertension--an electron paramagnetic resonance study. 828 19

Accumulated evidence has suggested that several sodium pump inhibitors, similar to cardiotonic steroids, are present in the human body. Ouabain-like factor, the most appealing candidate, has been found to be increased with high sodium intake and hypervolaemia, and in essential hypertension, mineralocorticoid hypertension, and pregnancy-induced hypertension. Furthermore, blocking the action of ouabain-like factor with digibind or a novel anti-ouabain agent lowers blood pressure in several models of hypertension. Several important questions remain, however, before it can be concluded that ouabain-like factor is indeed involved in the regulation of sodium homeostasis and blood pressure.
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PMID:Ouabain-like factor. 952 22

We have previously demonstrated that a 12 kD hypertension-associated protein (HAP) is elevated in essential hypertension and that this protein has the characteristics of natriuresis, inhibition of Na-K-ATPase, displaces 3H-ouabain from binding sites, and is vasoconstrictive in vitro. In the present study, plasma from 101 patients were examined [25 normals (N)<age 50, 13 N >age 50, 7 with acute congestive heart failure (CHF), 24 with chronic renal failure (CRF), on dialysis, 5 with idiopathic hyperaldosteronism (PA) and 27 with essential hypertension, untreated (EHT)]. Plasma was extracted with 32% acetonitrile, then analyzed by DELFIA for marinobufagenin and ouabain. In addition, from 32 patients (6 N <50, 6 N >50, 5 CHF, 5 CRF, 6 EHT, and 4 PA) SDS gradient gels were obtained. The 12 kD bands were extracted, analyzed for Na-K-ATPase inhibition, marinobufagenin and ouabain, and compared to 14 kD and 21 kD bands. Marinobufagenin was found to be elevated in CRF, EHT, PA and CHF. Ouabain was increased only in PA. When the relative optical densities of the 12 kD and 21 kD bands were contrasted, CRF, PA, and EHT were found to be increased and CHF to be decreased in the 12 kD band, with no discernible changes in the 21 kD bands. Following extraction of the bands, Na-K-ATPase inhibitory activity measured 38% in 18 pooled 12 kD bands, with essentially no activity found in the 14 kD or 21 kD bands. Thus only the 12 kD HAP band possessed all of the attributes of natriuretic hormone.
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PMID:Simultaneous measurement of marinobufagenin, ouabain, and hypertension-associated protein in various disease states. 968 18


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