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

Intracellular sodium, potassium, and free calcium concentrations were investigated in lymphocytes of 30 patients with essential hypertension and 30 normotensive controls. All subjects were placed on a diet containing 8 to 10 g of sodium chloride per day. Lymphocyte sodium concentration was higher in hypertensive patients than in normotensive controls (19.8 +/- 1.8 vs 18.4 +/- 1.8 mmol/kg wet weight; p less than 0.01), whereas lymphocyte potassium concentration was similar in both groups. Lymphocyte free calcium concentration was also higher in hypertensive patients than in normotensive controls (134.6 +/- 13.2 vs 120.2 +/- 16.4 nmol/L; p less than 0.01). There was a positive correlation between lymphocyte sodium and free calcium concentrations in normotensive controls, in hypertensive patients, and in the subjects combined (r = 0.59, p less than 0.01; r = 0.71, p less than 0.001; and r = 0.70, p less than 0.001, respectively). Lymphocyte potassium concentration was not related to lymphocyte sodium or free calcium concentration in each group. In patients with essential hypertension, intracellular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r = -0.66, p less than 0.001; r = -0.60, p less than 0.001, plasma norepinephrine concentration. These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity.
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PMID:Intralymphocytic sodium and free calcium and plasma renin in essential hypertension. 329 77

In this review, we first summarized the evidence from animals and man for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for a role for dietary sodium in the genesis of hypertension is strongest in those subjects with impaired ability to excrete sodium due to organic renal disease or mineralocorticoid excess. Here restriction of dietary sodium promptly lowers arterial pressure. Its role in the genesis of essential hypertension is still controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in blood pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep blood pressure under control. We next considered the mechanism of the pressure response to dietary sodium chloride, concentrating upon the increase in extracellular fluid volume, potassium depletion, and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic factor. We next summarized the evidence for a primary role for dietary potassium in the genesis of hypertension and pointed out that certain subsets of subjects with a high incidence of hypertension also have a lower dietary potassium intake. Some investigators find that dietary potassium supplementation lowers blood pressure in established hypertension. This may result from natriuresis and from vasodilation subsequent to stimulation of Na+, K+-ATPase in vascular smooth muscle and adrenergic nerve terminals. We then considered practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension. The review concludes with comments on their possible roles in the prevention of hypertension.
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PMID:Dietary sodium and potassium in the genesis, therapy, and prevention of hypertension. 329 78

The validity of the captopril test for primary aldosteronism (PA) was tested in patients with surgically verified PA (n = 12) or essential hypertension (EHT, n = 20) with different levels of sodium intakes. The patients were scheduled on 7 days each of three regimes of the prepared diet containing 34, 120 and 340 mEq of sodium chloride per day, and the captopril test was repeated in each period. For the test, captopril (50 mg) was administered orally at 9:00 A.M. after 1 hour of rest in a supine position, and venous blood samples were obtained before and 90 min after drug administration. Plasma aldosterone concentration (PAC; ng/dl) and plasma renin activity (PRA; ng/ml/h) were measured by radioimmunoassay. Under the three different sodium intakes, a PAC/PRA ratio greater than 20 at 90 min after captopril administration was sufficiently sensitive (0.95, 19/20) and specific (0.92, 55/60) to identify PA. Similarly, PA was associated with a PAC above 15 ng/dl 90 min after captopril. There were no complaints associated with the antihypertensive effects of the drug even when patients were sodium-restricted. These results confirmed that the captopril test is safe and useful for screening out-patients for PA, independent of individual differences in sodium intake.
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PMID:Effects of sodium intake on the captopril test for primary aldosteronism. 330 11

We investigated whether the anionic component of an orally administered sodium salt can influence the salt's capacity to increase blood pressure. In five men with essential hypertension in whom blood pressure was normal with restriction of dietary sodium chloride to 10 mmol per day (0.23 g of sodium per day), oral administration of sodium chloride for seven days, 240 mmol per day (5.52 g of sodium per day), induced significant increases in systolic and diastolic blood pressures, of 16 +/- 2 and 8 +/- 2 mm Hg (mean +/- SEM), respectively (P less than 0.05). An equimolar amount of sodium given as sodium citrate induced no change in blood pressure. Replacing supplemental sodium chloride with an equimolar amount of sodium as sodium citrate abolished the increase in blood pressure induced by sodium chloride. Both salts induced substantial and comparable sodium retention, weight gain, and suppression of plasma renin activity and plasma aldosterone, but supplemental sodium chloride increased plasma volume and urinary excretion of calcium, whereas sodium citrate did not. These preliminary findings demonstrate that the anionic component of an orally administered sodium salt can influence the ability of that salt to increase blood pressure, possibly by determining whether the salt induces an increase in plasma volume. Our observations in a small group of men with salt-sensitive hypertension will require confirmation in larger numbers of patients of both sexes.
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PMID:"Salt-sensitive" essential hypertension in men. Is the sodium ion alone important? 330 53

It is clear that salt is known to be a health hazard from the ancient times. Sodium intake, which was minimal during evolution, increased significantly with the civilization. The rise in prevalence of hypertension in populations with increased consumption of salt suggested a casual relationship. However, several of these studies showed conflicting results. Many investigators agree that salt-sensitive persons often have a family history of hypertension. Such individuals possess a sodium transport inhibitor in the arterial smooth muscle cells, which affects their sodium handling (as compared to other persons). However, many of the putative defects related to sodium can be dissociated from blood pressure and sodium consumption status. It is possible that calcium defects of deficiency of potassium and magnesium follow hypertension and sodium status. For example, the pressure response to sodium chloride may be dissociated from sodium, which may be secondary to adverse effects of chloride on calcium homeostasis. Clinical studies also indicate that the role of sodium is controversial in hypertension. Sodium restriction can benefit salt-sensitive persons and might not otherwise. However, most authorities believe that moderation of salt intake to a relevant extent is justifiable. Large scale, long-term intervention studies and shortterm clinical studies in different communities, in the light of recently investigated dietary factors, are necessary to establish the role of sodium in essential hypertension.
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PMID:Does sodium play an adverse role in hypertension? 331 98

The mechanism by which excessive sodium chloride intake raises blood pressure has not been fully clarified. The present study was therefore undertaken in patients with essential hypertension to investigate the possible role of an intracellular calcium-dependent mechanism in salt sensitivity. The difference in mean blood pressure between a week of low sodium chloride diet (3 g/day) and a week of high sodium chloride diet (20 g/day) was studied in relation to the intracellular free calcium concentration in lymphocytes and an acute hypotensive response to a 10-mg sublingual dose of nifedipine in 12 inpatients. Sodium chloride loading induced significant increases in mean blood pressure (from 111 +/- 12 to 122 +/- 11 mm Hg; p less than 0.01), intracellular free calcium in lymphocytes (from 133 +/- 13 to 145 +/- 9 nmol/L; p less than 0.01), and the hypotensive response to nifedipine (from 19 +/- 6 to 31 +/- 10 mm Hg; p less than 0.01). In addition, serum total calcium concentration was decreased while urinary calcium excretion was increased. The elevation of mean blood pressure was closely and positively correlated with the increase in intracellular free calcium concentration (r = 0.71, p less than 0.05) and the increase in the hypotensive effect of nifedipine (r = 0.91, p less than 0.01) after sodium chloride loading. However, changes in these values had no relation to the change in serum concentration or urinary excretion of calcium. These data suggest that change in the cellular calcium-dependent vasoconstriction mechanism may be associated with salt sensitivity of patients with essential hypertension.
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PMID:Role of cellular calcium in salt sensitivity of patients with essential hypertension. 339 81

Hypotensive activity of labetalol therapy alone or in combination with the diuretic agent oxodolin or with low-sodium diet (about 110 mmol/day) and potassium cooking salt substitute "Sanasol" (60% sodium chloride, ammonium chloride, calcium gluconate, magnesium asparaginate, etc.) was studied in 67 patients with second- or third-stage essential hypertension and 14 patients with nephrogenic hypertension. Central hemodynamic changes were assessed by means of radiocardiography and tetrapolar rheography. Combined treatment had better hypotensive effect in moderate and severe hypertension (diastolic arterial BP above 110 mm Hg). The diuretic-labetalol combination made possible a 25-45% reduction in the adrenoblocker dose. The effect of combined hypotensive treatment was similar in patients with different central hemodynamic types. Low-sodium diet with potassium substitute was well tolerated by the patients.
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PMID:[Potentiation of the hypotensive effect of labetalol in hypertensive patients treated to maintain sodium balance in the body]. 357 27

To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. ANG II was also in nine patients with essential hypertension eating a low sodium diet. In preliminary studies, the effects of nifedipine, 20 mg p.o., on blood pressure and plasma renin activity were determined. Sensitivity to infused ANG II was calculated as the slope of the linear regression of the increase in diastolic blood pressure (DBP) expressed as a function of the ANG II infusion rate (mm Hg/ng ANG II/kg/min). During intake of a high sodium diet (Na, 200 mEq/day) both drugs significantly (p less than 0.05) reduced ANG II sensitivity, while on a low sodium diet (10 mEq Na), neither drug reduced ANG II sensitivity. There was a significant (p less than 0.001) inverse correlation between the initial ANG II-DBP sensitivity and the change in sensitivity induced by the calcium channel blocking drugs in normal subjects (r = -0.78) and in hypertensive patients (r = -0.70). Five hypertensive patients had greater than normal ANG II-DBP sensitivity that was significantly (p less than 0.05) reduced by nifedipine. Calcium infusion did not affect the ANG II-DBP sensitivity on either diet. The results suggest that in normal subjects increased DBP responses to ANG II, induced by an increase in sodium intake, are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel blocking drugs nifedipine and diltiazem. In hypertensive patients on a low sodium diet, increased DBP responses to ANG II infusion were blocked by nifedipine, indicating they are at least partly mediated by increased extracellular to intracellular calcium flux.
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PMID:Effect of sodium balance and calcium channel blocking drugs on blood pressure responses. 362 78

A decrease in sodium intake or an increase in potassium intake reduces blood pressure (BP) in people with essential hypertension. Additional potassium prevents, in sodium-sensitive people and rats, the rise in BP caused by extra sodium chloride. In people with a diastolic BP between 90 and 100 mm Hg, dietary reduction of sodium to 80 mmol/day and dietary increase of potassium to 90 mmol/day caused a fall in BP of 5.1/4.2 and 3.6/3.1 mm Hg, respectively, greater than was observed in the control group. There was a negative interaction between the two diets when used together with a BP change of 4.0/3.6 mm Hg. The fall in BP with sodium restriction was not reversed by the addition of sodium chloride and a similar fall in BP was not achieved with potassium chloride. It is possible that the response is due to some other factor. A strong correlation existed between the change in urine Na:K and the fall in BP. This study indicates that a reduced sodium or an increased potassium diet will reduce BP and should be considered for the initial management of essential hypertension.
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PMID:Comparative studies of reduced sodium and high potassium diet in hypertension. 369 45

To study the role of calcium movements in mediating the effects of sodium chloride on the response of plasma aldosterone to angiotensin II (AII), we administered calcium channel-blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes before and after AII infusion. AII was also infused in 13 patients with essential hypertension eating a high sodium diet. In preliminary studies, the effects of nifedipine (20 mg, orally) on blood pressure, PRA, plasma aldosterone, and plasma cortisol concentrations were determined. Sensitivity to infused AII was calculated as the slope of the linear regression of the increase in plasma aldosterone as a function of the AII infusion rate (nanograms per dl/ng AII/kg X min). During sodium restriction (10 meq Na/day), both drugs significantly (P at least less than 0.05) reduced AII sensitivity. During the high sodium diet (200 meq Na/day), only diltiazem decreased AII sensitivity, and the reduction was less (P less than 0.05) than that during the low sodium diet. There was a significant (P less than 0.001) inverse correlation between the initial plasma aldosterone sensitivity to AII and the change in sensitivity induced by the calcium channel-blocking drugs in normal subjects (r = -0.89) and hypertensive patients (r = -0.70). Five hypertensive patients had greater than normal aldosterone sensitivity to AII, which was significantly (P less than 0.05) reduced by nifedipine. Calcium infusion increased the aldosterone sensitivity to AII during the low sodium diet, but not during the high sodium diet. The results suggest that in normal subjects, increased plasma aldosterone responses to AII induced by reduction in sodium intake are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel-blocking drugs nifedipine and diltiazem. In hypertensive patients eating a high sodium diet, increased aldosterone responses to AII infusion were blocked by nifedipine, indicating that they are at least partly mediated by increased extracellular to intracellular calcium flux.
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PMID:Effect of sodium balance and calcium channel-blocking drugs on plasma aldosterone responses to infusion of angiotensin II in normal subjects and patients with essential hypertension. 376 Jan 14


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