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

Findings from hypertension research indicate that dietary sodium chloride (NaCl), Na+, and Cl- independently influence blood pressure, electrolyte metabolism, and hormone secretion. In this context, we examined the effects of NaCl, Na+, and Cl- depletion, respectively, on the development of saline preference (salt appetite) in rats. Male Wistar rats were given a normal diet (1% NaCl) for 15 days and tested for salt appetite using a two-bottle choice test, one bottle containing water and the other 0.3 M saline. The animals were then divided into three groups (n = 11/group): one group received low NaCl, another received a Na(+)-deficient, normal-Cl-diet (low Na+), and a third received a Cl(-)-deficient, normal-Na+ diet (low Cl-). Salt appetite was again tested after 19 days on these diets. Both NaCl and Na+ depletion stimulated saline intake (P less than 0.01), whereas salt appetite did not change in the low-Cl- group. Water intake was not influenced by the regimens. In addition, no alterations were noted for weight, systolic blood pressure, plasma Na+ concentration, or blood pH. Dietary Cl-depletion, however, significantly reduced plasma Cl- concentration (P less than 0.05), and reduced plasma potassium in relation to rats depleted in Na+ (P less than 0.05). Plasma renin activity and urinary aldosterone were elevated in low-NaCl and Na(+)-depleted rats relative to the Cl(-)-depleted group (P less than 0.05). These results suggest that salt appetite is increased by dietary Na+ deficiency but not by Cl- deficiency. Salt appetite may be controlled by central or peripheral systems specifically sensitive to Na+ or by hormonal changes characteristic of Na+ depletion, such as the activation of renin and aldosterone observed in the low-NaCl and low-Na+ groups.
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PMID:Selective effects of sodium and chloride depletion on salt appetite in rats. 188 49

We all agree to the importance of the salt restriction in the prevention and the treatment of hypertension. But it is not easy to teach the way to reduce salt intake in each person or patient. And we also not confident that how long could they maintain the low salt diet. In this study we investigate following problems, 1) Can the salt intake be reduced in public population? 2) Can blood pressure be lowered by reducing salt intake in mildly hypertensive individuals? 3) If the desired changes are obtained, can they be preserved for a long time? and 4) Are there any difference in the amount of the salt intake between hypertensives and normotensives? One hundred and forty subjects from 23,940 people in whom borderline to mild hypertension was found at group medical examinations in each district, where a total of 29,940 people were examined, were registered to a educational course of new salt-restriction program. Salt intake was estimated from salt measurement in 24-hour urine samples. Educational program was composed of many lectures, sampling party and individualized consultations about dietary problems, using an original dietary questionnaire list. The results were as follows: In short-term (2.5 months) after the initial education, sodium intake reduced from 235.1 +/- 110.8 mmol/day to 161.4 +/- 85.0 mmol/day (p less than 0.001). The systolic and diastolic blood pressure also fell significantly in borderline hypertensives (from 148 +/- 7/87 +/- 5 mmHg to 141 +/- 12/85 +/- 7 mmHg, p less than 0.001) and hypertensives (from 165 +/- 13/99 +/- 8 mmHg to 157 +/- 15/95 +/- 8 mmHg, p less than 0.001) but they did not change in normotensives (from 133 +/- 6/80 +/- 6 mmHg to 131 +/- 9/82 +/- 8 mmHg). In long-term (range from 12 to 36 months) observation, low salt diet (167.6 +/- 72 mmol/day) and a fall in blood pressure were also maintained in borderline (142 +/- 2/85 +/- 7 mmHg, p less than 0.001) to hypertensive population (156 +/- 14/93 +/- 8 mmHg, p less than 0.001), and in the normotensive population, no change in blood pressure was observed (134 +/- 13/82 +/- 9 mmHg). Hypertensives tended to show higher sodium intake than normotensives (206 +/- 101 mmol/day vs. 199.0 +/- 96, p less than 0.005), and also show higher sodium/potassium ratio than normotensives and borderline hypertensives (4.3 +/- 2.3 vs. 3.6 +/- 1.6 and 3.8 +/- 1.8, p less than 0.005).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A population study of long-term salt restriction in mild hypertensives]. 191 27

We distinguish determinants of individual blood pressure elevations and those which influence shape and location of entire population distributions, i.e. epidemiological determinants. Individual and epidemiological determinants are not necessarily the same. Identification of the latter may be used to develop population wide prevention strategies that carry a great potential of reducing the public burden of cardiovascular morbidity and mortality. Salt has long but controversially been suspected as a major etiologic agent in hypertensive populations. For the first time the INTERSALT study tried in a systematic and standardized way to assess the salt-BP association in individuals and across 52 populations in 32 countries. The observed within center relations to systolic and more so to diastolic BP were largely inconsistent in direction and magnitude indicating probable non-uniformity of the salt effect. In this case, statistical pooling of single effect estimates may have lead to invalid conclusions. Across center analyses found no relevant relation of median sodium excretion to median BP values or hypertension prevalence and hence no evidence for salt as an epidemiologic BP determinant. It is concluded that the INTERSALT evidence is not sufficient to warrant salt restriction in the general population. This contrasts with consistent and quantitatively relevant individual and population associations of body mass index with blood pressure in INTERSALT. Considering its potentially multifactorial preventive effects, BMI reduction seems to be a more pragmatic public health measure for the German population.
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PMID:Are the conclusions of INTERSALT applicable to the German population? 192 Dec 45

Dopamine in urine is derived substantially from renal uptake and decarboxylation of 3,4-dihydroxyphenylalanine (dopa), and increases in excretion of dopa normally parallel increases in excretion of dopamine during salt loading. Since patients with salt-sensitive hypertension may have decreased urinary excretion of dopamine during dietary salt loading, the present study was designed to evaluate the response of dopa to salt loading. Sixteen inpatients with normal-renin essential hypertension ate a constant metabolic diet containing 9 mmol/day sodium for 7 days, followed by the same diet but containing 249 mmol/day sodium for 7 days. Salt sensitivity was defined as an increase in mean arterial pressure of 8 mm Hg between the diets; on this basis, nine patients were salt-sensitive and seven, salt-resistant. The rate of urinary dopa excretion was significantly higher in the salt-sensitive patients throughout the study (mean rates 132 +/- 13 nmol/day in the salt-sensitive group and 78 +/- 9 nmol/day in the salt-resistant group for the 14 days of observation, p less than 0.01). When dietary sodium intake was increased to 249 mmol/day, urinary dopa excretion increased significantly more in salt-sensitive patients than salt-resistant patients. At the end of the high salt diet, dopamine excretion was significantly attenuated in the salt-sensitive patients, despite higher rates of dopa excretion. Thus, the urinary ratio of dopamine to dopa was decreased in salt-sensitive patients, regardless of salt intake.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Nov
PMID:High urinary dopa and low urinary dopamine-to-dopa ratio in salt-sensitive hypertension. 193 64

The major differences that have been recognized between black and white hypertensives are primarily epidemiologic, with hypertension being more prevalent, having an earlier onset, and having more severe sequelae in the black population. The cause of the problem in both black and white people remains obscure, but it appears that a difference in sodium handling may contribute to the particular hemodynamic and hormonal profile of black hypertensives. Salt sensitivity, expanded plasma volume and low renin levels have been the hallmark of the black hypertensive. Complications such as stroke and left ventricular hypertrophy remain the major sequelae of this disease in blacks. Finally, a current study confirmed the improved efficacy of antihypertensive therapy in blacks to diuretics and calcium channel blockers and a somewhat lower efficacy profile to angiotensin converting enzyme inhibitors and beta blockers, although the latter classes of agents have shown better response in blacks than previously thought.
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PMID:Hypertension in blacks. 194 90

The relation between sodium and blood pressure is a centuries-old question. A substantial body of epidemiological and experimental data has accumulated that strongly implicates NaCl as having a causal role in the genesis of arterial hypertension. Prospective studies that have been performed in diverse populations that have manipulated NaCl exposure by diet or infusion have repeatedly documented an NaCl pressor effect. Further, similar studies in biracial populations have also demonstrated a greater prevalence of "salt sensitivity" in blacks compared with whites. The reasons for this observation are not entirely clear; however, intrinsic or hypertension-induced renal abnormalities that limit natriuretic capacity, reduced Na+,K(+)-ATPase pump activity, other membrane ion transport disturbances, differential exposure to psychological stressors, greater insulin resistance, and dietary factors (reduced Ca+ and K+ intake) have all been suggested as possibly playing a role. Salt sensitivity appears to be a widespread phenomenon. However, it is critically important to determine what factors account for racial differences in salt sensitivity. Moreover, the prevalence of salt sensitivity in the general population is unknown. Current definitions of salt sensitivity are varied and unidirectional. In comparison with bidirectional criteria (blood pressure increase with salt loading and blood pressure decrease with salt restriction), they are probably inadequate to identify salt-sensitive individuals who manifest less extreme blood pressure change after dietary sodium or plasma volume manipulations. More sensitive criteria for diagnosing salt sensitivity will facilitate a better understanding of racial and ethnic differences in the prevalence of salt sensitivity.
Hypertension 1991 Jan
PMID:Racial and ethnic modifiers of the salt-blood pressure response. 198 88

Salt (NaCl) is a ubiquitous component of diets in developed countries. A major reason for this is that people judge many salted foods as more palatable than the same foods without salt. Because recent evidence indicates that an acceptable salt substitute is unlikely, an understanding of the behavioral and sensory factors involved in maintaining high salt preference is a prerequisite to successful programs aimed at reducing intake. Although little evidence exists for a genetic determination of individual differences in consumption and preferred level of salt, more research in this area is necessary. Considerable data support the view that the optimal level of salt in the diet is determined in part by the level an individual is currently consuming; increasing or decreasing customary salt intake, as long as the salt is tasted, increases or decreases the preferred level of salt in food. Although these data are consistent with a hypothesis that optimal salt preferences are learned, other data, from both animal models and human developmental studies, suggest that salt preference has an innate component. Furthermore, early experience with low or high salt diets may have a long-term impact on preferred salt levels. Liking for salt, similar to liking for sweets, has an innate basis that can be modified by individual experience.
Hypertension 1991 Jan
PMID:High salt intake. Sensory and behavioral factors. 198

The effects of the mineralocorticoid antagonist mespirenone on the development and maintenance of aldosterone-induced hypertension in Sprague-Dawley rats has been studied. Uninephrectomized saline-drinking male Sprague-Dawley rats were injected with either 0.2 ml olive oil, 50 g aldosterone, 1 mg mespirenone, 50 g aldosterone plus 500 g mespirenone, or 50 g aldosterone plus 1 mg mespirenone, each dissolved in 0.2 ml olive oil. Administration of aldosterone alone significantly increased the systolic blood pressure (SBP) from a control value of 114 +/- 3.6 to 162 +/- 4 mmHg by the end of the 3-wk experimental period. Mespirenone given alone had no effect on SBP. However, mespirenone given in combination with aldosterone reversed the hypertension caused by aldosterone in a dose-dependent manner. Saline consumption and urinary output were slightly increased in aldosterone-treated rats compared with the other groups, but the body and organ weights were comparable in all groups. Microscopic examination of kidney and heart showed no abnormalities due to mespirenone. These results suggest that in vivo administration of mespirenone to Sprague-Dawley rats effectively prevents the aldosterone-induced hypertension.
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PMID:Effect of a new mineralocorticoid antagonist mespirenone on aldosterone-induced hypertension. 199 30

When the function of the renin system is inhibited, blood pressure becomes more dependent on changes in sodium and water balance. Diuretics alone and sodium restriction alone are additive to converting enzyme inhibitor therapy. However, it is not known if these two ways of reducing sodium balance are additive in the presence of established converting enzyme inhibition. We therefore performed a double-blind crossover study of the effects of moderate sodium restriction in 21 patients with essential hypertension who were already being treated with the combination of a converting enzyme inhibitor and a diuretic. After 1 month of captopril (50 mg twice daily) and hydrochlorothiazide (25 mg once daily) therapy, with their usual sodium intake, average supine blood pressure was 147/96 +/- 5/3 (SEM) mm Hg 2 hours after treatment. Patients then reduced their sodium intake to around 80-100 mmol/day for the remainder of the study. After 2 weeks of sodium restriction, they entered a double-blind, randomized, crossover study of Slow Sodium (100 mmol sodium/day) compared with Slow Sodium placebo, while continuing sodium restriction and the above treatment. During the double-blind study, after 1 month of treatment with captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium placebo, supine blood pressure 2 hours after treatment was 138/88 +/- 4/2 mm Hg (24-hour urinary sodium 104 +/- 11 mmol). After 1 month of captopril (50 mg twice daily), hydrochlorothiazide (25 mg once daily), and Slow Sodium tablets, supine blood pressure 2 hours after treatment was 147/91 +/- 5/2 mm Hg (p less than 0.05; 24-hour urinary sodium 195 +/- 14 mmol).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Sodium restriction in hypertensive patients treated with a converting enzyme inhibitor and a thiazide. 204 42

Cardiac output, blood volume, total peripheral resistance, and renal blood flow were measured in awake salt-sensitive and salt-resistant Dahl rats on normal rat chow (1% NaCl) and on high salt (8% NaCl) diets. Rats were studied after 4, 8, and 46 weeks on a 1% NaCl diet and after 4 and 8 weeks on an 8% NaCl diet. Salt-sensitive rats on 8% NaCl for 4 weeks developed systolic hypertension; by 8 weeks they developed greater systolic and also diastolic hypertension. Salt-resistant rats on 8% NaCl remained normotensive throughout the studies, although renal resistance decreased (p less than 0.05). At 4 weeks, hypertension in salt-sensitive rats on 8% NaCl was caused by increased blood volume and cardiac output (p less than 0.05), with normal total peripheral resistance. At 8 weeks, hypertension was due to increased total peripheral resistance (p less than 0.05); cardiac output was below normal despite persistent elevation of blood volume (p less than 0.05). Salt-sensitive rats on 1% NaCl for 46 weeks were hypertensive, with elevated total peripheral resistance (p less than 0.05); cardiac output decreased (p less than 0.05), whereas blood volume remained unchanged. Salt-resistant rats on 1% NaCl remained normotensive with no charges in hemodynamics. Salt-sensitive rats on 8% NaCl for 4 weeks had an increase in renal vascular resistance but no significant change in nonrenal resistance or total peripheral resistance. The increased total peripheral resistance in salt-sensitive rats on 8% NaCl for 8 weeks and on 1% NaCl for 46 weeks was a reflection of increases of both renal and nonrenal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Dual hemodynamic mechanisms for salt-induced hypertension in Dahl salt-sensitive rats. 204 50


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