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

The effects of an intravenous infusion of physiological saline on plasma atrial natriuretic peptide (ANP), guanosine 3' 5' monophosphate (cGMP) concentrations, and on urinary cGMP and sodium excretion were studied in 13 patients with essential hypertension, class I according to WHO criteria, and in 10 healthy subjects. It was found that the groups did not differ as to basal and infusion-induced plasma ANP and cGMP and basal urinary cGMP and sodium excretion, but the sodium chloride infusion resulted in a significantly greater urinary cGMP and sodium excretion and creatinine clearance in hypertensive than in control subjects. The results of this study demonstrate that patients with essential hypertension respond to an intravenous sodium chloride load not only with exaggerated natriuresis, but also with augmented urinary cGMP excretion. The latter finding may in part be due to a greater glomerular filtration of cGMP, but increased renal contribution cannot be excluded. Apart from the possible stronger intrarenal effect of ANP on cGMP production in patients with hypertension, independent direct effect of volume expansion on cGMP excretion and modified activity of other cGMP generating systems may all be responsible for the higher urinary cGMP excretion in essential hypertension.
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PMID:Exaggerated natriuresis induced by sodium chloride infusion in essential hypertension is accompanied by an exaggerated urinary 3' 5' guanosine monophosphate excretion. 841 56

The natriuretic response that accompanies an acute or a chronic sodium load results, in a large part, from dopamine produced by the renal proximal tubules. This paracrine/ autocrine effect of dopamine, mediated by occupancy of renal tubular dopamine D1 receptors, is impaired in spontaneous hypertension. Disruption of the D1A receptor gene in mice increases blood pressure. The D3 receptor is also present in renal proximal tubules and juxtaglomerular cells, and it may be an inhibitor of renin release. Disruption of the D3 receptor gene in mice also increases blood pressure, but the ability to excrete a sodium chloride load is not impaired. Thus, selective manipulation of dopamine receptor subtypes might aid in studies of the pathogenesis of essential hypertension and the design of novel drugs to treat high blood pressure.
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PMID:What we can learn from the selective manipulation of dopaminergic receptors about the pathogenesis and treatment of hypertension? 893 15

Over several million years the human race was programmed to eat a diet which contained about 15 mmol of sodium (1 g of sodium chloride) per day. It is only five to ten thousand years ago that we became addicted to salt. Today we eat about 150 mmol of sodium (9-12 g of salt) per day. It is now apparent that this sudden rise in sodium intake (in evolutionary terms) is the most likely cause for the rise in blood pressure with age that occurs in the majority of the world's population. Those which consume less than 60 mmol/day do not develop hypertension. The reason for the rise in sodium intake is not known but it is probable that an important stimulus was the discovery that meat could be preserved by immersion into a concentrated salt solution. This seemingly miraculous power endowed salt with such magical and medicinal qualities that it became a symbol of goodness and health. It was not until 1904 Ambard and Beaujard suggested that on the contrary dietary salt could be harmful and raise the blood pressure. At first the idea did not prosper and it continues to be opposed by a diminishing band. The accumulated evidence that sodium intake is related to the blood pressure in normal man and animals and in inherited forms of hypertension has been obtained from experimental manipulations and studies of human populations. The following observation links sodium and hypertension. An increase in sodium intakes raises the blood pressure of the normal rat, dog, rabbit, baboon, chimpanzee and man. Population studies have demonstrated a significant correlation between sodium intake and the customary rise in blood pressure with age. The development of hypertensive strains of rats has revealed that the primary genetic lesion which gives rise to hypertension resides in the kidney where it impairs the urinary excretion of sodium. There is similar but less convincing evidence in essential hypertension. The kidney in both essential hypertension and hypertensive strains of rats share a number of functional abnormalities most of which are capable of impairing sodium excretion. Essential hypertension would appear to be as much a renal disturbance related to the intake of sodium as hypertension secondary to renal disease.
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PMID:[Sodium and hypertension]. 895 9

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 +/- 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 +/- 1.9 to 105.0 +/- 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 +/- 2.4 to 2.2 +/- 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.
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PMID:Change in blood pressure during altered sodium intake is not associated with calciotropic hormone level. 930 30

The relationship between (excessive) use of sodium chloride and the blood pressure is still equivocal. Blood pressure responses to alterations in dietary salt consumption vary greatly between individuals, which has led to the concept of salt sensitivity. Although the mechanisms which determine the degree of salt sensitivity are not fully understood, the renin-angiotensin system seems to play a key role. A relative inability of this system to respond promptly to alterations in salt intake may underlie the development of salt sensitivity. By administering drugs which block the renin-angiotensin system to patients with essential hypertension, blood pressure is rendered more sensitive to the effects of salt restriction and (or) diuretic treatment.
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PMID:[Salt sensitive blood pressure and the renin-angiotensin system in hypertension]. 955 Aug 12

We examined the circadian rhythm of urinary sodium excretion and the effects of sodium restriction on rhythm in both dipper and nondipper types of essential hypertension. Patients (n = 26) with essential hypertension were maintained on relatively high- (10 to 12 g/d of sodium chloride) and low-sodium (1 to 3 g/d) diets for 1 week each. On the last day of each diet, 24-hour blood pressures (BPs) were measured every 30 minutes noninvasively with an automatic device, and on the last 3 days, urinary samples were collected for both daytime (7:00 AM to 9:30 PM) and nighttime (9:30 PM to 7:00 AM). Eight patients were classified as dippers based on a more than 10% reduction in mean arterial pressure (MAP) from daytime to nighttime on a high-sodium diet, and 18 patients were classified as nondippers. A nocturnal decrease in urinary sodium excretion rate (U(Na)V) on the high-sodium diet was observed in dippers (from 7.5 +/- 2.1 during the day to 5.3 +/- 2.5 mmol/h at night; P < 0.0001), but not in nondippers (6.7 +/- 2.1 v 7.6 +/- 2.3 mmol/h; not significant). In nondippers, the night-day ratio of sodium excretion was significantly reduced from 1.2 +/- 0.4 to 0.8 +/- 0.3 (P < 0.003) by sodium restriction; at the same time, the night-day ratio of MAP was reduced from 0.98 +/- 0.04 to 0.93 +/- 0.05 (P < 0.05). In dippers, the night-day ratios of MAP and U(Na)V were not affected by sodium restriction, and both ratios remained constant at less than 1. Before sodium restriction, the night-day ratio of sodium excretion correlated with that of MAP (r = 0.78; P < 0.0001), whereas there was no significant correlation (r = -0.05) after sodium restriction. These findings showed that the circadian rhythm of renal sodium excretion differed between the two types of essential hypertension. The enhanced nocturnal natriuresis and diminished nocturnal BP fall on a high-sodium diet, recognized in nondippers, were both normalized by sodium restriction, resulting in circadian rhythms with nocturnal dips in U(Na)V and BP.
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PMID:Circadian rhythm of natriuresis is disturbed in nondipper type of essential hypertension. 991 64

There is evidence of impaired renal sodium excretion in salt-sensitive African Blacks. A decreased rate of renal sodium chloride (NaCl) excretion, low plasma renin activity and a tendency to elevated blood pressure are the hallmarks of salt sensitivity. Recent evidence indicates that increased proximal and distal tubular fluid reabsorption in some tropical residents may explain the impaired sodium excretion in these people. In this study of a cohort population, we speculated that subjects selected from that population might be salt-sensitive. We therefore measured the sodium balance in 10 normotensive male subjects over 10 consecutive days, after they had ingested a normal or a high amount of sodium, as NaCl (salt) in their diet. We quantified their renal sodium excretion rate by phenomenological analysis of their sodium balance data. We also measured plasma renin activity for 7 consecutive days in a separate group of 6 male and 4 female subjects in order to assess the state of their renin/angiotensin system. We selected all our subjects from a cohort population of 269 subjects randomly selected from a community known to have a high prevalence of primary hypertension. Our data on two separate groups of subjects from the same cohort population revealed delayed renal sodium excretion with t1/2 of about 5 days, compared to published data for normal individuals with t1/2 of less than 24 h. Also, plasma renin activity levels were low. Hence, our subjects are salt-sensitive. Quantification of their renal impairment is important for various reasons: it heightens one's appreciation of the problem of salt retention in African Blacks who are salt-sensitive and it also underlines the importance of the need for further research into the benefits of dietary salt restriction for reducing cardiovascular mortality in African populations, as has been done in some Western countries.
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PMID:Impairment of renal sodium excretion in tropical residents--phenomenological analysis. 1046 16

Severe short-term sodium restriction or extreme sodium loading may alter glucose tolerance and insulin resistance in patients with hypertension, but it is unclear whether variations in sodium intake within the clinically observed range affect glucose tolerance. To examine this issue, 21 patients with primary hypertension with average sodium excretion of 116+/-55 mEq/day were randomized to consecutive 4-week periods of placebo therapy and sodium chloride supplementation 2 g four times a day in a single-blind crossover study design. A 75-g oral glucose tolerance test (GTT) with simultaneous insulin levels was performed at the end of each intervention period. For the group as a whole, urinary sodium excretion increased on sodium chloride to 267+/-118 mEq/day versus control (placebo) phase of 135+/-53 mEq/day, P < .001. Total glycemic response in the oral GTT (area under the glucose curve) was 8.0% lower during sodium supplementation, P < .001. Secondary analysis revealed that the effect of sodium was noteworthy in 1) type 2 diabetic subjects (n = 8), 2) sodium-sensitive subjects (n = 10), and 3) nondiabetic subjects receiving antihypertensive drug treatment (n = 6). The total insulinemic response to oral GTT was also lowered by sodium loading among diabetic subjects. Thus, an abundant sodium intake may improve glucose tolerance and insulin resistance, especially in diabetic, salt-sensitive, and or medicated essential hypertensive subjects.
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PMID:The effect of sodium supplementation on glucose tolerance and insulin concentrations in patients with hypertension and diabetes mellitus. 1146 50

Microcirculation was studied with biomicroscopy of the eye bulbar conjunctiva's vessels in 50 patients with essential hypertension stage II aged 60-80 years. They took half baths with sodium chloride mineral water at Irkutsk health resort "Angara". The treatment resulted in improvement of perivascular and intravascular end blood flow.
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PMID:[Status of microcirculation in elderly hypertensive patients during treatment with sodium chloride baths]. 1189 73

The pathogenic role of angiotensin II (ANG II), dietary sodium chloride, sympathetic activation, obesity and aldosterone in the development of structural vascular changes (SVCs) in hypertension is considered from three perspectives (criteria): their utility in predicting hypertension and its complications (predictability); the effect of their inhibition or removal on the reversal of SVCs (reversibility); and their ability to induce SVCs in experimental animals (reproducibility). Only ANG II meets all three criteria. Importantly, ANG II increases preglomerular vascular resistance by inducing structural changes in renal cortical resistance arteries and arterioles. High salt intake, by dilating and thereby stiffening some arteries, may play a role in the development of systolic hypertension with aging, but does not produce structural changes in renal cortical resistance vessels. While high circulating levels of norepinephrine are associated with SVCs, the experimental evidence for the role of sympathetic nerve stimulation in the development of SVCs is inconclusive. Obesity is associated with hypertension, but is not known to be associated with SVCs. Salt-loading is required for aldosterone to produce SVCs, but vascular pathology in this experimental model differs from that in benign essential hypertension. The findings of this review indicate that SVCs in extra-renal sites by themselves do not lead to hypertension; structural changes in renal cortical arteries and arterioles that increase preglomerular vascular resistance are needed. Progressive trophic stimulation of preglomerular resistance vessels by itself may lead to hypertension. ANG II is prime candidate for such stimulus.
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PMID:Pathogenesis of structural vascular changes in hypertension. 1516 59


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