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

1. Chronic hypertension was induced in Wistar rats with intact kidneys by subcutaneous implantation of 50 mg of deoxycorticosterone acetate (DOCA) in wax and addition of sodium chloride (9 g/l) to the drinking water. 2. The development of DOCA/salt hypertension, as monitored by tail-cuff plethysmography, was prevented by: (a) destruction of the peripheral adrenergic nerves with neonatal administration of guanethidine (80 mg/kg subcutaneously for the first 14 days postnatally); (b) bilateral stellate ganglionectomy; (c) oral administration of the beta-adrenoreceptor antagonists propranolol or atenolol (1 mg day-1 kg-1) during the period of DOCA/salt treatment. 3. The dose of DOCA used was sufficient to inhibit the atrial Uptake2 pathway completely: this process appears to participate in termination of action of neurally released noradrenaline in the heart. 4. It is suggested that this model of DOCA/salt hypertension is due to adrenergic enhancement of cardiac output in the presence of an increased sodium load. The enhancement may be partly due to deficient myocardial inactivation of noradrenaline.
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PMID:Dependence of deoxycorticosterone/salt hypertension in the rat on the activity of adrenergic cardiac nerves. 3 42

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and medullar zones of the kidneys, a decrease of the sodium and potassium gradient in the renal tissue. Adaptation to hypoxy is noted so cause a decrease in the interventricular factor, in the width of the glomerular zone of the adrenal glands, in the sodium concentration in the erythrocytes, an increase in the mass of the medullar layer of the kidneys, and an increase in the sodium and potassium gradients. When adaptation to hypoxy is combined with the effect of desoxycorticosterone-acetate-salt, hypertension develops to a lower degree than in non-adapted animals.
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PMID:[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia]. 12 78

The present study was performed to investigate whether blood pressure of salt-loaded rats was influenced by the diet. Salt-loaded rats of Wistar strain were fed a high protein high fat diet or a high carbohydrate diet from the age of one month. The experiment was designed so that the intake of sodium chloride was equal in two groups. The body weight on the 14th week of the experiment was 394 +/- 15 g (Mean +/- SE) in the high protein high fat group, and 348 +/- 13 g in the high carbohydrate group. Blood pressure measured weekly by a tail plethysmographic method rose gradually and reached 176 +/- 5 mmHg (Mean +/- SE) on the 14th week in the high carbohydrate group. It was significantly higher than that (127 +/- 7 mmHg) of the high protein high fat group. The pressor responses to angiotensin and noradrenalin were also examined to investigate the mechanism through which salt hypertension was produced more easily by feeding a high carbohydrate diet. These responses to both drugs tended to be greater in the high carbohydrate group, but the differences between the two groups was not significant.
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PMID:Effects of energy-containing nutrients on blood pressure of salt-loaded rats. 44 12

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

After an ischaemia lasting 1 hour as well as after an extreme hypertension lasting 210 minutes in the kidney of a rat a significant increase of the renin activity in the juxtaglomerular apparatus was found. By chronic load with sodium chloride was tried to produce a decrease of renin. In contrast to an ischaemic lesion the kidneys of the animals loaded with salt revealed a better ischaemia tolerance than those of the unloaded animals. This is expressed by a significantly increased total blood supply and cortical blood supply. On the two experimental conditions a change of the distribution of the blood supply in favour of the inner compartments of the kidneys may be observed. In the oxygen histogram of the surface of the kidney the salt-loaded kidneys reveal a better oxygenation before and after the ischaemic lesion. The kidneys loaded before show an essentially more insignificant decrease of the urine excretion than the unloaded ones.
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PMID:[Chronic sodium chloride load--a possibility for the increase of tolerance for ischemia in the kidney]. 48 65

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.
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PMID:Role of central catecholamines in the control of blood pressure and drinking behavior. 49 58

We studied the combined effect of subpressor amounts of angiotensin and long-term sodium chloride infusion on arterial pressure in 16 dogs for periods of 2--8 weeks. In dogs receiving 3.5 liters of isotonic NaCl daily, but no angiotensin, the arterial pressure increased an average of only 3 mm Hg. When angiotensin was infused continuously at a rate of 5 ng/kg per min (a rate too small to cause an observable immediate increase in pressure, subsequent infusion of 3.5 liters of saline daily then increased the pressure by 39 mm Hg. The urinary output of sodium increased to the same extent in both instances, that is, there was no extra sodium loss because of the elevated pressure. This suggests that the angiotensin significantly blocked the normal "pressure natriuresis" usually seen with such large increases in pressure. However, the plasma aldosterone levels during angiotensin infusion were not found to be different from those in the absence of angiotensin. Therefore, we have suggested that the tendency of the kidneys to retain sodium under the influence of angiotensin was probably caused mainly by a direct effect of angiotensin on the kidney itself. Such a direct renal sodium-retaining effect also could be a contributing factor in the marked hypertension that results from salt administration in the presence of small amounts of angiotensin.
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PMID:Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog. 68 54

The high sodium-low potassium environment of civilized people, operating on a genetic substrate of susceptibility, is the cardinal factor in the genesis and perpetuation of "essential" hypertension. The noxious effects begin in childhood, when habits of excess salt consumption are acquired at the family table, and are perpetuated by continuing habit and by increasing use of convenience and snack foods with artificially high concentrations of sodium and low levels of potassium. Present methods of food preparation leach out the protective potassium. Extradietary sodium chloride is a condiment not a requirement. Some primitive populations clearly preferred potassium chloride to sodium chloride. Chronic expansion of extracellular fluid volume induced by excess salt consumption causes the central and peripheral circulatory regulatory mechanisms to work at cross purposes, resulting in increased arterial pressure. The protective effect of potassium is dramatic and easily demonstrable in animals and man but its mechanism is not known. It cannot be entirely a direct effect on blood pressure because rats protected with extra potassium against a moderately high salt intake live much longer than control rats but have the same elevated blood pressures. In hypertension with a demonstrable "cause," the high sodium-low potassium environment makes a bad matter worse. In nature, feral man and his forebears were not confronted with excessive sodium and deficient potassium; indeed, the reverse was the case. Evolution has provided powerful mechanisms for conserving sodium and eliminating potassium, but no efficient physiologic mechanisms for conserving potassium and eliminating excess sodium. Most laboratory animal "control" diets contain an amount of sodium that fully suppresses aldosterone secretion, and the same is true of the "average" diet of the American people. Inadequate attention to dietary sodium and potassium makes many studies in both animals and man of uncertain validity. Internally, essential hypertension is an exceedingly complex mosaic of physiologic interactions. Viewed from outside, it is a disorder for which genetic material sets the stage; excessive sodium precipitates it and perpetuates it. Extra salt makes all forms more rapidly progressive and accelerates the onset of terminal events; extra potassium is everywhere protective. When an entire population eats excessively of salt, hypertension will develop among those genetically susceptible, but epidemiologic studies of salt versus blood pressure will not show a relation of salt to hypertension. This is the saturation effect. Low sodium diets are therapeutically effective but generally regarded as an impossible or an unnecessary nuisance. Effective prevention programs must be instituted at as early an age as possible. The efficacy of a prophylactic/therapeutic low sodium-high potassium diet should be weighed against the uncertain hazards of a lifetime of pill taking.
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PMID:High sodium-low potassium environment and hypertension. 79 67

Elderly participants in Title VII congregate feeding programs in Indianapolis can be characterized generally as being retired, usually living alone, and often reporting some disease condition, particularly arthritis, hypertension, and/or heart disease. On an average weekday, the nutrient intake of these people, except for zinc, approximated the amounts suggested in the Recommended Dietary Allowances. Fifty-nine per cent of the subjects consumed less than two-thirds of the allowance for zinc. Generally, they consumed over half of their allowances for eight nutrients at the site meal. The nutritional significance of apparent low intakes of dietary zinc among subjects is not clear. Eleven per cent had hair zinc levels below 100 mcg. per gram, but none were below 70 mcg. Therefore, on the basis of hair zinc levels, none could be absolutely calssified as zinc deficient. Although hair zinc levels were not correlated to dietary zinc intake, they were inversely correlated to dietary calcium and fat intake. Taste acuity by these elderly participants was generally less than that reported for young adults. However, women had greater taste acuity for sodium chloride than men. Sixteen per cent of the subjects were particularly insensitive to the taste of sodium chloride. Finally, there was no correlation between taste acuity and dietary zinc intake.
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PMID:Zinc nutriture of elderly participants in an urban feeding program. 83 Jul 6


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