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

The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Blood pressure (BP), plasma renin concentration (PRC) and exchangeable sodium (NaE) were measured in eighteen patients with advanced chronic renal failure, nine hypertensives and nine normotensives, and in seven normal subjects (a) 6 days after a fixed sodium intake of 10 mmol/day, and (b) 6 days after a fixed sodium intake of 150 mmol/day. Mean NaE was 14-19% higher in the hypertensives compared with the normotensives and values of NaE correlated significantly to values of mean BP. No significant differences were present in PRC between the groups of patients and controls on either of the sodium regimens and no correlation was found between BP and PRC. However, average decreases of PRC in the hypertensives on high sodium intake, 33-34%, were significantly lower than the corresponding values of 69-71% in the normotensive patients and controls, respectively. Furthermore, the percentage changes of PRC on high sodium intake correlated significantly to mean BP as well as to NaE. These results suggest that renin release is relatively unresponsive to different sodium intakes in hypertension following chronic renal failure. This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately' increased in relationship to the sodium excess.
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PMID:The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure. 14 27

Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. Plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. Autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.
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PMID:Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia. 19 43

The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5--2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10--50 fold in all groups during the ACTH test. Aldo rose transiently 2--4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention aTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.
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PMID:Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension. 21 19

The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
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PMID:The toxicity of salt. 35 85

1. Neonatal sympathectomy with 6 hydroxy-dopamine (6-OHDA) was used as a tool to assess the significance of an increased sympathetic vascular tone for the development of high blood pressure in stroke-prone spontaneously hypertensive rats. After administration of 6-OHDA the rise in blood pressure was blunted for the following 9 weeks until innervation was re-established. 6-OHDA-treated rats retained more sodium and had larger plasma and blood volumes than sham-treated rats. 2. Catecholamines in plasma were increased 2-10-fold immediately after sympathectomy, but their concentrations were subnormal on day 7. Eight weeks after sympathectomy plasma noradrenaline and dopamine were not elevated, but plasma adrenaline has increased twofold. 3. The reactivity of resistance vessels to noradrenaline was markedly enhanced and the neuronal uptake and metabolism of noradrenaline were still reduced 8 weeks after neonatal sympathectomy. 4. These results confirm the significance of an intact sympathetic nervous system for the development in these rats. Sodium retention and increased plasma and blood volume may be considered as a compensatory mechanism for the vasodilatation resulting from decreased vasomotor tone.
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PMID:Effect of neonatal sympathectomy by 6-hydroxydopamine on volume and resistance regulation in stroke-prone spontaneously hypertensive rats. 54 Apr 31

Although the healthy infant can tolerate the range of sodium intakes normally present in the variety of diets offered in Britain without developing hypernatraemia or evidence of serious disease, there is enough evidence to suggest that care is required in the amount of sodium given to babies. The consequence of excessive sodium intake may be short term or long term. The most common short term complication is hypertonic dehydration. In the long term, the fear is that high intakes of sodium in early infancy may predispose to hypertension in later life, though this is as yet unproven.
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PMID:Sodium intake and health in infancy. 56 78

Body fluid volumes, cardiac output, PRA and pressor responses to angiotensin II (AT) and norepinephrine (NE) were compared between untreated patients with essential hypertension aged younger than 35 (EH-I) and those aged older than 36 years (EH-II). Men blood volume, total body water and extracellular volume were not significantly different between the patients with essential hypertension and normotensive subjects. There were no difinite differences in each volume between the EH-I and EH-II patients either. However, the distribution of blood volume was significantly larger in the essential hypertensive patients than in the normotensive subjects, suggesting that the changes in blood volume might not be homogenous in essential hypertension. In addition, blood volume was noted to have a significant inverse correlation with PRA. Cardiac output at rest was slightly but not significantly less in the EH-I and EH-II groups than in the normotensive group. A decline in blood pressure following 'bed-rest' was accompanied by a decrease in total peripheral resistance index (TPRI). Thus, elevated peripheral vascular resistance seems to be responsible for the mild to moderate hypertension even in the younger patients. PRA and its increases in response to standing or furosemide were normal in the EH-I patients, while they were markedly suppressed in the EH-II patients as compared to the age-matched normotensive subjects. In addition, PRA had a significant inverse correlation with the blood pressure and the scores of the severity of hypertension in the patients with essential hypertension. Thus, it seems likely that low renin in essential hypertension is secondary to long-lasting hypertension. Pressor response to AT significantly correlated with mean blood pressure and that to NE did so with 24 hours' urinary sodium excretion in essential hypertensive patients. The influence of aging on the pressor responses were obscure: the relationships of the pressore responses to blood pressure or to urinary sodium excretion were not different between the EH-I and EH-II groups. The examinations were repeated in 16 patients with essential hypertension (16 to 48 year-old) in 11 to 30 days after the initial study. Twelve of the 16 patients had declines in blood pressure and TPRI at the second study. In 7 of the patients whose blood pressure declined following 'bed-rest', there were significant decreases in pressor response to AT and in blood volume and a significant increase in PRA (group A). The other 5 patients showed a significant decrease in PRA and an enhanced pressor response to NE (group B). The blood volume in the group A was significantly larger than that in the group B at the initial study. It is suggested that the cause of essential hypertension is not homogeneous in that the increased vascular resistance may have been attributed to sodium excess in some patients and to an increased sympathetic activity in others. Some additional factors remain to be taken into account to clarify the complicated aspects of essential hypertension.
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PMID:Comparisons of body fluid volumes, plasma renin activity, hemodynamics and pressor responsiveness between juvenile and aged patients with essential hypertension. 87 Jul 21

1. Restriction of dietary salt intake does not affect the development or maintenance of hypertension in rats with unilateral renal ischaemia whether the contralateral kidney is present (Goldblatt 2 model) or not (Goldblatt 1 model). 2. Acute dietary salt depletion induces a similar loss of sodium and fall in body weight with little change in blood pressure in both normal and hypertensive rats. 3. Excision of the ischaemic kidney in rats with short-term (less than 50 days) Goldblatt 2 hypertension restores the mean blood pressure to normal, whereas Goldblatt 1 hypertensive rats show only a partial response. Previous salt depletion of this model enhances the blood pressure response to nephrectomy. 4. Sodium retention plays no part in the development or maintenance of Goldblatt 2 kidney hypertension. However, although sodium retention is normally involved in the Goldblatt 1 model, hypertension can develop in the absence of dietary sodium.
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PMID:Influence of sodium restriction upon two models of renal hypertension. 96 57

1. In eighteen subjects with mild to moderate hypertension the effectiveness of the new vasodilator drug L6150 (Lepetit) was studied. Its mechanism of action was identified by systemic and renal blood flow measurements and by estimating changes in plasma renin and aldosterone concentration and plasma volume. The reflexly induced hyperkinetic circulatory state could be completely corrected by adding propranolol or prevented by pretreatment with the latter drug. 2. Sodium retention was an invariable phenomenon. It was not due to a stimulation of the reninangiotensin-aldosterone axis since plasma aldosterone was significantly decreased, presumably as a consequence of plasma volume expansion.
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PMID:Haemodynamic and endocrinological changes during anti-hypertensive treatment with a new vasodilator substance (L6150) and propranolol. 107 88

This paper describes an infant with gastroenteritis, who developed hypertension and oedema after administration of inaccurately prepared oral glucose salt solution. The renin aldosterone system was suppressed in this child and it was suggested that this may be a factor in the development of hypernatraemia when abnormal water losses occur in infants fed on hyperosmolar feeds. Unless salt can be given accurately in small amounts it may be safer to advise feeds of glucose only in infants with mild diarrhoea.
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PMID:Hypertension, oedema, and suppressed renin aldosterone system due to unsupervised salt administration. 119 Aug 14


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