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

We compared normal values for human venous norepinephrine (NE) and epinephrine (E) as reported in the literature with values determined in this laboratory and we measured and contrasted NE levels in patients with primary and secondary hypertension. Analysis of published data from many laboratories involving more than 800 supine, resting, healthy subjects indicated an average circulating level of venous NE of 260 pg/ml and of E, about 35 pg/ml. Supine levels of NE normally double when normal subjects stand for 5 min. This simple test provides one assessment of overall sympathetic nervous system integrity. Levels of catecholamines have been extensively studied in essential hypertension but much less so in secondary hypertension. Of the groups we studied with secondary hypertension (diabetes mellitus, primary hyperaldosteronism, polycystic kidney disease, chronic bilateral renal parenchymal disease, and unilateral renal arterial stenosis), only the group with renal parenchymal disease had supine NE levels significantly higher than the control group. Patients with essential hypertension and diabetes had a blunted increase in NE on standing. Plasma levels of NE do not reliably differentiate these groups of secondary hypertension from one another or from patients with primary hypertension.
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PMID:Plasma catecholamine levels in normal subjects and in patients with secondary hypertension. 669 Mar 38

Lactic dehydrogenase (LDH), a cytosolic enzyme found in neural and endocrine tissue, was measured in serum and tumor tissue of 15 patients with pheochromocytoma, a neuroendocrine neoplasm. Mean serum total LDH activity was higher in patients with pheochromocytoma than in patients with essential hypertension, normotensive control subjects, or those with various other categories of secondary hypertension. The prominent isoenzyme was LDH type 3. Their pheochromocytoma tissue, as well as normal human adrenal tissue, also contained LDH, maximally type 3; the amount of LDH in tumors far exceeded that in normal adrenal glands, suggesting that the tumor tissue is the source of the excessive serum LDH in these patients. While a large percentage of false-negative results (40%) does not render serum LDH activity a reasonable screening test for pheochromocytoma, and even though the true-positive rate is high (100%), we cannot yet recommend that hypertensive patients with high serum LDH activity undergo investigation for this tumor.
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PMID:Lactic dehydrogenase activity in human pheochromocytoma. 684 29

In erythrocytes, the extrusion of a cell sodium load is accomplished by the ouabain-sensitive sodium-potassium pump and by the furosemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. The precise characterization of these transport pathways requires the determination of the turnover rates of cation translocation and the affinities for substrates and effectors. The preliminary results of such kinetic study in essential hypertension is reported here. An abnormally low rate of net sodium extrusion by the sodium-potassium co-transport system was observed in essential hypertensive patients and in a high proportion of their young normotensive offspring. A normal cotransport system found in secondary hypertensive subjects devoid of familial history of hypertension confirmed that the abnormal cotransport system is not the consequence of high blood pressure per se. At the molecular level, the cotransport abnormality seems to be consecutive to a diminished apparent affinity for intracellular Na+. A 20-40% increase in the rate of net sodium extrusion by the sodium-potassium pump seems to compensate for the abnormal cotransport in erythrocytes from some young normotensive subjects born of essential hypertensive parents and from some benign essential hypertensive subjects. No difference could be detected between the passive sodium permeability of erythrocytes from hypertensive subjects and normotensive controls. In conclusion, essential hypertension seems to be associate with an inherited defect in the apparent affinity for intracellular Na+ of the sodium-potassium cotransport system. We propose therefore the laboratory study of this system for (i) the distinction between essential and secondary hypertension and (ii) the preventive investigation of young normotensive subjects in hypertensive families.
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PMID:Abnormal erythrocyte Na+ K+ cotransport system, a proposed genetic marker of essential hypertension. 694 39

A polypeptide fraction isolated from the urine of normotensive subjects lowers the blood pressure (BP) in a rabbit bioassay (mean BP decrease 33.8% +/- 0.6%, SEM). Patients with primary hypertension exhibit reduced or no activity (mean BP decrease 8.8% +/- 1.2%). In contrast, patients with secondary forms of hypertension show activity like normotensives (mean BP decrease 33.4% +/- 1.0%). The results of the bioassay in the two patient groups correlate well with the family incidence of hypertension (68% and 37% for primary and secondary hypertension respectively). Cases with borderline hypertension fall into two groups; a larger one with vasoactivity inthe bioassay and lower family incidence of hypertension; and a smaller group reacting like patients with primary hypertension. Only the latter group may represent an initial stage of primary hypertension. In normotensive children and young men, an inactive fraction was found in 31% and 28% respectively. These inactive groups had twice the family incidence of hypertension compared to the groups with vasoactivity. These results suggest the existence of a possible genetic marker of primary hypertension and may offer the possibility to detect the disease before its manifestation.
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PMID:Defect in the excretion of a vasoactive polypeptide fraction A possible genetic marker of primary hypertension. 694 42

Plasma renin, adrenaline and noradrenaline were measured by the respective radioenzymic and radioimmunological methods in 69 patients with essential hypertension, 40 patients with secondary hypertension from chronic parenchymatous renal disease and in 18 normotensive controls. Plasma levels of adrenaline and noradrenaline were not statistically different in primary secondary hypertension and were comparable with normotensive controls. Compared with secondary hypertension, only 4% of patients with primary hypertension had a marginally raised plasma noradrenaline, compared with normotensive subjects, only 6% had a definitely raised plasma noradrenaline level. Though absolutely normal, noradrenaline in high renin essential hypertension was significantly higher than in low renin essential hypertension; it correlated neither with age nor blood pressure. Plasma adrenaline was reduced in about 30% of patients with primary and secondary hypertension, leading to a positively skewed frequency distribution; plasma adrenaline correlated positively with heart rate (p less than 0.001), pulse pressure (p less than 0.01) and plasma noradrenaline (p less than 0.01) and negatively with diastolic blood pressure (p less than 0.05). Supine plasma catecholamine levels do not demonstrate differences in adrenergic tone in primary and secondary hypertension and do not add any new evidence for an increased sympathetic tone in primary hypertension. In fact, plasma adrenaline is suppressed in about 30% of patients with primary and secondary hypertension.
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PMID:[Plasma adrenaline and noradrenaline in essential and renal hypertension (author's transl)]. 702 Feb 60

The relationship between blood pressure (BP) and the renin-angiotensin-aldosterone system was studied in a stratified random sample (n=120) of 49-year-old men selected from a BP screening and covering a wide range of BPs. Only subjects not on antihypertensive treatment were included. None had malignant or secondary hypertension. Plasma renin activity, plasma concentrations of angiotensin II, aldosterone, sodium, potassium and noradrenaline and the 24-hour urinary excretions of sodium, cortisol and noradrenaline were determined. Of these variables, only p-aldosterone was significantly correlated wtih BP, both in the whole study group (R=0.22, p less than 0.02, n=119) and in the subjects with the highest BP range (R=0.36, p less than 0.02, n=30). Of the clinical groups compared, the hypertensive subjects had significantly higher mean p-aldosterone than the borderline and normotensive subjects. Multiple regression analysis showed that the 24-hour urinary excretion of noradrenaline was the factor most strongly correlated to p-aldosterone, suggesting that the sympathetic nervous system might stimulate aldosterone secretion. Our findings indicate that aldosterone may be of importance for the development and maintenance of essential hypertension.
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PMID:Blood pressure in relation to the renin-angiotensin-aldosterone system. 705 60

Abnormal erythrocyte Na+ transport has been reported in patients with essential hypertension and some first-degree relatives. The two major techniques now employed for estimating Na+ transport--Na+/Li+ countertransport and Na+/K+ cotransport--are rather intricate and time consuming. Furthermore, the precise nature of the transport processes being measured is not clear. We have developed a simpler, more direct technique based on measurement of 22Na+ accumulation by erythrocytes. 22Na+ uptake by red cells from patients with essential hypertension averages twice normal. Indeed, of 21 patients with essential hypertension, only 2 patients had values within the upper end of the normal range. In 12 patients with secondary hypertension and no family history of essential hypertension, erythrocyte 22Na+ accumulation was within normal limits. Control experiments indicate that our technique for estimating red cell 22Na+ uptake is highly reproducible and shows little day-to-day variation. This procedure for the assessment of erythrocyte Na+ transport should be useful in differential diagnosis and the presymptomatic identification of individuals genetically prone to essential hypertension.
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PMID:Assessment of red cell sodium transport in essential hypertension. 705 49

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

An abnormally low sodium-potassium net flux ratio in erythrocytes was recently described in human essential hypertension. We have confirmed this finding in 65 patients with essential hypertension who were compared with 33 normotensive controls born of normotensive parents. In 23 other subjects with documented secondary hypertension and normotensive parents, the sodium-potassium net flux ratio was found to be similar to that in the controls. The erythrocyte test thus appears to be of interest in distinguishing between essential and secondary hypertension. Severe renal failure itself reduces the flux ratio and would therefore distort the results of this test.
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PMID:Laboratory distinction between essential and secondary hypertension by measurement of erythrocyte cation fluxes. 735 8

This paper describes experiments showing that one of the pathways of sodium transport across the red-cell membrane, sodium-lithium countertransport, is faster in patients with essential hypertension than in control subjects. This transport system accepts only sodium or lithium and is not inhibited by ouabain. The maximum rate of transport shows inherited differences. The mean maximum rate of sodium-lithium countertransport was found to be 0.55 +/- 0.02 (mean +/- S.E.M.) mmol (liter of red cells X hour)(-1) in a group of 36 patients with essential hypertension and 0.24 +/- 0.02 in 26 control subjects (P less than 0.001). The first-degree relatives of eight patients with essential hypertension and 10 control subjects had mean maximum rates of sodium-lithium countertransport of 0.54 +/- 0.05 and 0.23 +/- 0.02, respectively. Five patients with secondary hypertension had normal mean maximum rates of sodium-lithium countertransport. The relation between heritability of red-cell sodium-lithium countertransport and essential hypertension should be investigated further.
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PMID:Increased sodium-lithium countertransport in red cells of patients with essential hypertension. 735 9


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