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

In order to clarify the possible relationship between changes in blood pressure after salt loading, membrane sodium transport and renin profile, 19 patients with essential hypertension (8 patients with low renin hypertension and 11 patients with normal renin hypertension), admitted to our hospital, were studied. We also examined the correlation of changes in intracellular sodium concentration after salt loading between erythrocytes and lymphocytes. After a control period of one week, all subjects were placed on a low salt intake for one week followed by one week of a high salt intake. Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Percent changes in intracellular sodium concentration in erythrocytes inversely correlated with those in ouabain sensitive sodium efflux rate constant and positively correlated with those in intracellular sodium concentration in lymphocytes. These results suggest that an increase in sodium chloride sensitivity of blood pressure in patients with low renin hypertension may be due to the inhibition of Na+-K+ pump in vascular smooth muscle cell membrane.
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PMID:Sodium chloride sensitivity, intracellular sodium concentration in erythrocytes and lymphocytes, and renin profile in essential hypertension. 265 38

Factors which determine sodium chloride sensitivity, defined as the difference between the mean blood pressure after 1 week of a low sodium chloride diet (3 g/day) and that after 1 week of a high sodium chloride diet (20 g/day), were studied in 60 inpatients with essential hypertension using a multivariate analysis. The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. These data suggest that both intracellular sodium accumulation and inadequate suppression of the renin-angiotensin system may be independently involved in the elevation of blood pressure after sodium chloride loading. We could not find the independent importance of volume retention, hyperadrenergic activity or basal blood pressure in the sodium chloride sensitivity.
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PMID:Factors determining sodium chloride sensitivity of patients with essential hypertension: evaluation by multivariate analysis. 270 19

Changes in plasma levels of Na+, K+-ATPase inhibitors with salt loading were studied in eight patients with essential hypertension. By improving the assay method of Na+, K+-ATPase inhibitors to distinguish ouabain and vanadate, two types of inhibitors were detected in the plasma of patients with essential hypertension: One was ouabainlike and the other was nonouabainlike. The ouabainlike inhibitor was detected at low KCl concentrations (0.1 mM) in the assay buffer, and the nonouabainlike inhibitor was detected at a high KCl concentration (10 mM). By increasing dietary sodium chloride from 2 g/day for 5 days to 20 g/day for 6 days, systolic blood pressure increased significantly from 122 +/- 3.9 to 138 +/- 3.8 mmHg (p less than 0.005), whereas plasma renin activity decreased significantly from 3.9 +/- 0.8 to 0.8 +/- 0.3 ng/ml/hr (p less than 0.002). Under these conditions, the ouabainlike inhibitor increased significantly from 6.2 +/- 3.9% to 30.5 +/- 5.9% inhibition (p less than 0.005), after increasing dietary sodium. Furthermore, plasma level of the ouabainlike inhibitor correlated significantly with both systolic blood pressure (p less than 0.05) and daily urinary sodium excretion (p less than 0.01). In contrast, the plasma nonouabainlike inhibitor did not change with high sodium intake and did not correlate with blood pressure and daily urinary sodium excretion. These findings suggest that a ouabainlike inhibitor is involved in the maintenance of high blood pressure induced by high sodium intake in patients with essential hypertension. The role of the nonouabainlike inhibitor in blood pressure regulation is still unknown.
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PMID:Increase in plasma ouabainlike inhibitor of Na+, K+-ATPase with high sodium intake in patients with essential hypertension. 283 25

Dietary sodium restriction is increasingly regarded as important in the prevention and treatment of essential hypertension. However, low-sodium diets are frequently considered unpalatable and therefore unfeasible. The objectives of this study were to determine (a) whether hypertensives, treated and untreated, differ in saltiness taste perception from age-matched normotensive controls and (b) whether sodium reduction can be accomplished by substituting another taste stimulus without reducing apparent saltiness and palatability. Subjects included 72 hypertensives, 44 to 69 years old, divided among three treatment groups; 25 age-matched normotensive controls; and an additional 21 normotensives, 20 to 43 years old, to provide an age continuum for evaluating age effects. Taste responses were measured in terms of saltiness intensity and preference using tomato juice varying systematically in sodium chloride and citric acid content. No significant differences were found between normotensives and hypertensives. No significant effects were associated with blood pressure status, therapeutic regimen, age, sex, race, or anthropometric measurements. Both sodium chloride and citric acid were main effects for saltiness, allowing a trade-off between salt and acid. Addition of citric acid permitted 50% reduction of sodium content in tomato juice without disturbing palatability criteria. Results provide a model for modifying other processed foods.
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PMID:Taste responses to saltiness among hypertensive subjects under different therapeutic regimens. 285 7

Clinico-biochemical investigation of 76 persons with borderline arterial hypertension (BAH) aged 15 to 64 and 60 controls with assessment of some parameters of lipid, carbohydrate and water-salt metabolism was carried out. Gustatory sensitivity to sodium chloride was studied. Differences in the levels of these indices were revealed in patients with BAH with relation to the presence or absence of basal changes on ECG and fundus of the eye; there were also some differences in risk factors in BAH and essential hypertension.
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PMID:[Clinico-biochemical characteristics of persons with borderline arterial hypertension]. 296 28

A total of 50 patients with essential hypertension, I-II stages, were investigated to study changes in peripheral and intracardiac hemodynamics and myocardial contractility in moderate restriction of sodium chloride in "salt-sensitive" patients (SSP). In such patients (84% of all examinees) with mild arterial hypertension moderate restriction of SC consumption causes a sufficient antihypertensive effect determined by considerable improvement of peripheral hemodynamic indices and improvement of myocardial pump function and contractility, and in patients with moderate and severe hypertension it potentiates an antihypertensive effect and influence of drug therapy on hemodynamics. In non-SSP moderate restriction in SC consumption was ineffective. A sufficient antihypertensive effect in them resulted from the use of drug therapy at higher dosage than in SSP.
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PMID:[Changes in the hemodynamics and cardiac function of hypertension patients on moderate limited consumption of table salt]. 307 40

Fifteen unselected patients who had essential hypertension and whose average supine blood pressure when they were not receiving any treatment and their usual sodium intake was 162/107 mm Hg were treated with captopril 50 mg twice daily. After one month's treatment their supine blood pressure had decreased to 149/94 mm Hg. They were then instructed to reduce their sodium intake to about 80 mmol(mEq)/day. After two weeks of moderate sodium restriction they were entered into a double blind randomised crossover study comparing the effect of 10 Slow Sodium tablets (100 mmol sodium chloride) with matching placebo tablets while continuing to take captopril and restrict sodium in their diet. After one month of taking placebo their mean supine blood pressure was 137/88 mm Hg with a urinary sodium excretion of 83 mmol/24 h, while after one month of taking Slow Sodium tablets their mean supine blood pressure was 150/97 mm Hg (p less than 0.001) with a sodium excretion of 183 mmol/24 h. The mean supine blood pressure during moderate sodium restriction therefore decreased by 9% and correlated significantly with the reduction in urinary sodium excretion. These results suggest that the combination of treatment with a moderate but practical reduction in sodium intake and an angiotensin converting enzyme inhibitor is effective in decreasing the blood pressure in patients with essential hypertension. This combined approach overcomes some of the objections that have been made to salt restriction alone and to converting enzyme inhibitors alone.
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PMID:Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension: a double blind study. 310 61

The formation and action of intrarenal dopamine is reviewed, as also is the evidence for the use of gamma-L-glutamyl-L-dopa as a relatively renally specific dopaminergic pro-drug. 'Salt sensitive' patients with essential hypertension may have a fault in the renal mobilisation of dopamine by sodium chloride. This failure of sodium to dopamine coupling may be particularly prevalent in the Negro race.
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PMID:Dopamine, the kidney and essential hypertension studies with gludopa. 311 81

Six patients with essential hypertension underwent a randomized cross over design study to investigate the effect of supplementing a 10 mmol/day sodium diet for a period of 5 days with either 120 mmol sodium chloride (Slow Sodium, Ciba, Horsham, UK) or 122 mmol sodium in the presence of other anions, mainly phosphate (Phosphate, Sandoz, Feltham, UK). With both sodium salts, urinary sodium excretion was increased. The calculated amount of sodium retained was similar for both the sodium chloride and sodium phosphate periods. However, with the addition of sodium chloride to the low-salt diet, there were increases in supine mean blood pressure whereas with the addition of sodium phosphate no change in mean blood pressure occurred. The supine mean blood pressure after supplementation with sodium chloride (119.8 +/- 4.3 mmHg) was significantly greater than that after sodium phosphate (113.3 +/- 4.5 mmHg), similarly, the standing mean blood pressure was greater after addition of sodium chloride than of sodium phosphate (122.3 +/- 4.20 versus 115.4 +/- 3.0 mmHg). With both salts there were similar but non-significant increases in weight and reductions in plasma renin activity (PRA) and plasma aldosterone (PA).
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PMID:A randomized crossover study to compare the blood pressure response to sodium loading with and without chloride in patients with essential hypertension. 318 67

The significance of cellular calcium metabolism and systemic calcium balance in sodium chloride sensitivity was studied in 16 patients with essential hypertension and in 13 normotensive subjects. With changes in sodium chloride intake from 3 to 20 g/day, mean blood pressure, lymphocyte [Ca2+]i and the acute hypotensive response to nifedipine were increased in the hypertensive patients, but not in the normotensive subjects. Serum calcium concentration was decreased and urinary calcium excretion was increased in both groups. In the hypertensive patients, elevation of mean blood pressure was positively correlated with the increase in lymphocyte [Ca2+]i and with the enhancement of the hypotensive response to nifedipine, but it was not related to the change in serum or urinary calcium. These results suggest that enhancement of cellular-calcium-dependent vasoconstriction may lead to increased blood pressure following sodium chloride loading in patients with essential hypertension.
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PMID:Relationship of cellular calcium to salt sensitivity in patients with essential hypertension. 324 Dec 14


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