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

Thirty-seven subjects including 29 patients with essential hypertension (8 with labile and 21 with stable disease patterns) and 8 controls received salt and water loads. Sodium chloride was administered per os at a rate of 0.12-0.22 g bw, water at a rate of 20 ml bw. Before loads the measurements were taken of the total water content in the body and of the total metabolic sodium. Radiocardiography was employed to study the central hemodynamics. After sodium chloride load BP measurements were taken over 2 h, within the first 45 min every other 5 to 10 min. Sodium excretion with urine was measured hourly, whereas the changes in the central hemodynamics were evaluated every other 5 to 10 min. After water load BP measurements were taken for 1.5 h. Urine excretions were evaluated too. It was demonstrated that patients with labile and stable hypertension responded differently to salt and water loads. In the first case the increment of BP was similar to that seen in the controls, being measured by increases in the cardiac and stroke indices. In the second case BP rises were more prolonged and more significant than in the controls and occurred primarily at the expense of the high total peripheral resistance of the blood flow. There were two types of the response to salt load: the first one involved a rapid BP elevation (after 1 to 5 min) accompanied by the violent vegetative symptomatology and BP returning to normal after 20 to 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Salt and water loads and water-sodium metabolism in patients with hypertension]. 652 12

The effect of exercise of gradually increased intensity, i.e. 75 W for 20 min followed by 100 W for 20 min, on plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) was studied in young patients with essential hypertension and normotensive control subjects. During exercise without previous sodium loading PRC and PAC increased to the same degree in both hypertensives and normotensives during light exercise; PRC increased further significantly in the normotensives (63 to 72 microIU/ml (medians), P less than 0.01) but not in the hypertensives (46 to 51 microIU/ml) during heavy exercise. PRC and PAC were significantly correlated during both 75 W (rho = 0.633, P less than 0.05) and 100 W (rho = 0.635, P less than 0.05) exercise in the normotensives, but not in the hypertensives. During exercise after loading with 500 ml sodium chloride (0.85 mol/l) PRC and PAC increased in both hypertensives (28 to 42 microIU/ml, P less than 0.01; 0.11 to 0.53 nmol/l, P less than 0.01) and normotensives (22 to 33 microIU/ml, P less than 0.02; 0.12 to 0.34 nmol/l, P less than 0.01), although to a considerably lower degree than without previous loading. PRC and PAC were, however, significantly higher in the hypertensive than in the normotensive group after exercise. It is suggested that the responsiveness of the renin-aldosterone system is abnormal during exercise in young patients with mild essential hypertension, both without and with previous intravenous sodium loading.
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PMID:Responsiveness of the renin-aldosterone system during exercise in young patients with essential hypertension. 680 Aug 12

In vivo and in vitro studies have shown that renal formation of prostaglandins (PG), most probably at the juxtaglomerular complex represents an essential step for the mechanisms regulating the secretion of renin. PGs formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. Renal PG formation, especially that of PGE2, is reduced by high NaCl intake leading to a relative preponderance of PGF2 alpha at a reduced level of PG formation. These findings make renal PGs good candidates for participation in the renal regulation of sodium chloride balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG production might be involved in the etiology of high and low renin states. Thus, an impairment in the renal formation of vasodilating and renin-stimulating PGs as reflected by a blunted increase of urinary PGE2 excretion rate initially after furosemide in essential hypertensive patients could be the common denominator for both the blunted renin secretion and the increased vascular resistance which have been reported to be associated with this disease. Together with the observation of a positive correlation between PGF2 alpha formation (which enhances vasoconstriction following nerve stimulation) and blood pressure in human neonates, the findings suggest that abnormalities in the production of PGs whether due to genetic or as a result of environmental (NaCl) factors, could be involved in the development and in the natural history of essential hypertension.
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PMID:Renal prostaglandins, kidney function and essential hypertension. 700 57

The effect of dietary sodium intake (5 days' low salt, 4 days' high salt) on 24-h urinary prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) excretion, blood pressure (BP), and plasma renin activity (PRA) was evaluated in 16 patients with essential hypertension. Sodium restriction significantly increased urinary PGE2 excretion (p less than 0.05) from 151 +/- 76 to 328 +/- 94 ng/24 h, while high salt intake reduced renal PGE2 production to 114 +/- 41 ng/24 h (p less than 0.05). There was a moderate but not significant increase in urinary PGF2 alpha excretion on the low salt regimen, which was reversed under high salt diet. Systolic and diastolic blood pressure fell from 162 +/- 11 to 145 +/- 10 mm Hg, i.e., 102 +/- 6 to 90 +/- 9 mm Hg on low sodium intake (35 mEq/day) and returned to levels close to control after 4 days on a high salt diet (250 mEq/day). Under low salt conditions, PRA increased significantly (p less than 0.001) from 0.83 +/- 0.33 to 2.82 +/- 1.12 ng AI/ml/h and fell to 0.45 +/- 0.31 ng AI/ml/h on high salt regimen (p less than 0.001). The results demonstrate that dietary sodium chloride intake modulates renal PGE2 production in patients with essential hypertension. The depressed PGE2 production under high salt conditions may play a role in regulation of renal vascular resistance and influence sustainment of chronic hypertension disease.
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PMID:Sodium chloride as regulator of renal prostaglandin E2 production in patients with essential hypertension. 705 May 23

From at least 1928 until about 1940 essential hypertension was reported to be a rare disease among the population in Kenya and Uganda. Currently, it is 1 of the common causes of heart failure and a major cause of cerebrovascular disease in many hospitals in these 2 nations. Field data in these countries suggest that blood pressure rises during adult life, and essential hypertension occurs in salt-sensitive individuals, when sodium chloride daily intake is excessive. If the intake of potassium chloride is less than that of sodium chloride, and the intake of dietary fiber decreases much, as happens when diets are westernized, these may act as subsidiary risk factors. The East African diets are becoming more and more westernized. The 1st major dietary change involves the addition of much salt to low-salt unprocessed foods. With progressive westernization of diets the foods processed by manufacturers replace homegrown staples. These processed foods contain considerably more sodium, rather less potassium, and much less dietary fiber. While this multiple dietary change takes place, blood pressure levels, previously low and not rising with age, begin to rise during adult life. Essential hypertension, once rare, becomes common in sodium sensitive persons. Diets comparable in many respects to the 1930 Kikuyu diet are suggested to reverse essential hypertension. The therapeutic diet should be of low sodium chloride and should contain much unrefined high fiber high starch foods.
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PMID:From normotension to hypertension in Kenyans and Ugandans 1928-1978. 738 2

There is still a need of support for nonpharmacologic treatment of uncomplicated, mild-to-moderate essential hypertension. We investigated whether a low sodium-based diet implemented by a nutritionist could lower blood pressure and affect sympathetic activity. Middle-aged, otherwise healthy men with never-treated essential hypertension (n = 95) were randomized to an intervention group, a blood pressure control group, and a time control group. The intervention group was advised to use less sodium chloride in their diet, and if necessary, less saturated fat and decrease body weight. They attended regular clinic visits as did the blood pressure control group. After 1 year, the intervention group had achieved on average 72 mmol/24 h lower urinary sodium excretion (P < .001) and a decrease in body weight of 2.7 +/- 0.5 kg (P < .001). Both supine and standing mean blood pressure were on average 8 to 10 mm Hg lower after intervention compared with the two control groups (P < .001). Arterial plasma epinephrine, measured in all 40-year-old subjects (n = 30), decreased in parallel in all three groups (P < .05), indicating some habituation to the invasive procedure and clinic visits. However, the decrease in norepinephrine was significant (P < .001) only in the intervention group; it correlated with the weight loss (r = 0.76, P < .05) and was significantly higher (P < .05) than in both control groups. These results suggest that broad dietary advice (ie, low intake of sodium chloride, saturated fat and energy), implemented by a nutritionist, may have a significant blood pressure lowering effect and a favorable sympathicolytic effect in uncomplicated, mild-to-moderate essential hypertension.
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PMID:Effect of dietary counselling on blood pressure and arterial plasma catecholamines in primary hypertension. 754 96

Gastric inhibitory polypeptide (GIP) is one of the strongest insulinotropic gut factors. Its secretion is induced by oral (but not intravenous) glucose and it has been implicated in the pathogenesis of hyperinsulinemic states (NIDDM, obesity). To determine its relevance to hypertension, 54 subjects were studied: 26 normotensives (12 with and 14 without family history of essential hypertension), and 28 essential hypertensive subjects. Plasma glucose, serum insulin (IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. Venous blood was collected at baseline and every 15 min during a 3-h period. Baseline levels of glucose, IRI, and GIP were comparable in the three groups. At 30 min, however, IRI and GIP were higher in normotensives with a family history of hypertension and in established hypertensive versus control subjects. Both in normotensive and in hypertensive groups, glucose, IRI, and GIP responses to the meal were significantly correlated. Our data suggest the contribution of altered GIP secretion in the pathogenesis of hyperinsulinemia in essential hypertension.
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PMID:Hyperinsulinemia and hypertension. Do intestinal hormones play a role? 775 55

To examine the utility of the single-dose captopril test in detecting renovascular hypertension (RVHT), the authors measured peripheral plasma renin activity (PRA), before and thirty and sixty minutes after an oral dose of captopril (25 mg), in 28 patients with RVHT and 22 patients with high-renin essential hypertension (EHT) without renal artery stenosis who were consuming 8 grams of sodium chloride per day. There was considerable overlap of individual values in basal PRA between the two groups. Sixty minutes after captopril, PRA was higher in RVHT than in EHT patients (74.8 +/- 63.9 versus 15.1 +/- 11.9 ng/mL/hr, P < 0.01). With the cutoff point set at 16 ng/mL/hr, RVHT was detected with a sensitivity of 96% and a specificity of 77%. The discriminating power was also superior to that based on blood pressure response to angiotensin II analogue under sodium depletion, rapid-sequence intravenous pyelography, or renography. These results show that captopril-stimulated peripheral PRA is an adequate screening tool for detecting RVHT in a population with high-renin hypertension.
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PMID:Diagnostic value of captopril test in hypertensive patients with renal artery stenosis. 812 98

Age-related changes in cardiovascular regulatory mechanisms may affect blood pressure homeostasis during sleep and in the daytime. This study compared systemic hemodynamics during the daytime and sleep between 12 young or middle-aged patients (young, 42.1 +/- 13.9 years old, mean +/- SD, less than 56 years old) and 12 elderly patients with essential hypertension (old, 65.3 +/- 2.8, 60 to 70 years old). They were all hospitalized and placed on a diet containing approximately 7 g sodium chloride per day. Intra-arterial blood pressure and electrocardiogram were recorded for 24 hours, and electroencephalogram and electroophthalmogram were recorded during the night with a telemetric method. Cardiac output was measured with patients in the supine position by the cuvette method during the daytime and stage 3 or 4 sleep at night. The averaged 24-hour blood pressure was similar in the two groups (140 +/- 2 [SEM]/85 +/- 3 mm Hg in the young group and 144 +/- 4/81 +/- 2 mm Hg in the old group). The reduction in mean blood pressure during sleep was also comparable in both groups (-18 +/- 2 in the young group and -20 +/- 2 mm Hg in the old group). Cardiac index was smaller in the old group than the young group during both the daytime and sleep (daytime, 2.3 +/- 0.1 versus 3.2 +/- 0.2 [L/min]/m2, P < .01; sleep, 2.1 +/- 0.1 versus 2.6 +/- 0.2 [L/min]/m2, P < .01). The reduction in cardiac index during sleep was greater in the young than the old group (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic hemodynamics during sleep in young or middle-aged and elderly patients with essential hypertension. 830 24

The aim of this work was an evaluation of the effect of the acute hypervolemia induced by 90 min intravenous infusion of 1500 ml 0.9% NaCl (16.7 ml/min) on blood pressure, plasma concentration of the atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO), plasma renin activity (PRA) in patients with essential hypertension on the normal, low and high sodium intake. Twelve patients with noncomplicated essential sodium-sensitive arterial hypertension participated in the study. Sodium chloride infusions were performed three times: first--on the fifth day of normal daily sodium u intake (110-120 mmol/day), second--on the fifth day of low sodium intake (10-20 mmol/day), third--on the fifth day of high sodium intake (200-220 mmol/day). Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. The results suggest an impairment of the adaptive homeostatic mechanisms induced by an acute intravenous sodium load in patients with noncomplicated salt-sensitive essential hypertension ingesting high-sodium diet.
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PMID:[Effect of intravenous sodium chloride load on levels of atrial natriuretic peptide (ANP) and 3'5' guanosine monophosphate (cGMP) in plasma of patients with uncomplicated sodium-sensitive arterial hypertension maintained on different dietary sodium intake]. 838 45


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