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

Twelve hour urinary kallikrein excretion was measured in 18 healthy children of parents with essential hypertension and in 47 healthy children of parents without this disorder. No statistically significant difference was observed between the two groups of children.
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PMID:Urinary kallikrein excretion in children of parents with essential hypertension. 385 47

Abnormalities in the kallikrein-kinin system have been found in human and animal models of essential hypertension. The purpose of this study is to assess the kallikrein-kinin system in normotensive Dahl salt sensitive (S) and salt resistant (R) rats on a zero sodium diet. Urinary kallikrein was measured at 7 and 12 wk of age by different techniques. When kallikrein activity was assessed, by a kininogenase assay, S rats excreted 66% (P less than 0.001) and 75% (P less than 0.01) as much kallikrein as R rats at 7 and 12 wk of age. Using an artificial substrate method (Kabi S-2266), S rats excreted 30% (P less than 0.001) and 56% (P less than 0.05) as much kallikrein as R rats at 7 and 12 weeks, respectively. Using a technique to measure total kallikrein, S rats excreted 53% (P less than 0.001) and 65% (P less than 0.05) as much kallikrein as R rats at 7 and 12 wk of age. Normotensive S rats failed to increase maximally kallikrein activity or total kallikrein when the diet was switched from a .4% to a .0064% sodium chloride diet. There was no difference in inhibitors, as measured by the recovery of purified kallikrein added to S and R urine (56 +/- 21% vs. 53 +/- 13%). Km values for S and R urinary kallikrein were similar (3.1 +/- .5 X 10(-5) vs. 2.6 +/- .5 X 10(-5) M/liter). Trypsin-activatable kallikrein was equivalent in the S and R rats on the .0064% and .4% sodium chloride diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased total and active urinary kallikrein in normotensive Dahl salt susceptible rats. 385 74

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.
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PMID:Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia. 385

To assess the relationship between pressor and depressor factors in essential hypertension, the urinary excretion rates of prostaglandins E2 and F2 alpha, kallikrein, vasopressin and aldosterone were compared between 53 untreated hypertensive patients and 53 age- and sex-matched normotensive controls. Mean basal levels of plasma renin activity and of urinary prostaglandins, vasopressin and aldosterone were similar in both groups, but urinary kallikrein was significantly lower in the hypertensive patients. A weak relationship was found in the hypertensives between diastolic blood pressure, and vasopressin or aldosterone, and between vasopressin and prostaglandin E2, and in the normotensives between vasopressin and prostaglandin F2 alpha. In conclusion, these results do not provide evidence for an important imbalance between pressor and depressor factors in essential hypertension, as reflected by the urinary excretion of the major humoral factors and hormones involved in the regulation of blood pressure.
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PMID:Urinary excretion of renal prostaglandins, kallikrein, vasopressin and aldosterone in essential hypertension. 386 81

The effects of orally administered glandular kallikrein on urinary kallikrein, aldosterone and prostaglandin E (PGE) excretion, plasma renin activity (PRA), immunoreactive 6-keto PGF1 alpha and thromboxane B2 concentrations and platelet aggregation were studied in 12 patients with essential hypertension (EH). After a 2-week control period, each patient was given orally 450 KU/day of hog glandular kallikrein for 8 weeks. Urinary kallikrein, aldosterone and PGE excretion, and plasma 6-keto PGF1 alpha and thromboxane B2 concentrations were measured by radioimmunoassay. Platelet aggregation was measured by the addition of ADP, collagen or ristocetin with an aggregometer. Urinary kallikrein excretion and plasma 6-keto PGF1 alpha concentration were significantly decreased in patients with EH. There were no significant differences in PRA, urinary aldosterone excretion and plasma thromboxane B2 concentrations between control subjects and patients with EH. There was a significant decrease in blood pressure in patients with EH coinciding with significant increases of urinary kallikrein and PGE excretion and plasma immunoreactive 6-keto PGF1 alpha concentration after administration of glandular kallikrein. There was also a significant inhibition of platelet aggregation induced by collagen in these patients. Thus, a suppression of the kallikrein-kinin-prostaglandin system in patients with EH was found, and a decrease in blood pressure with an increment of urinary kallikrein, PGE excretion, plasma immunoreactive 6-keto PGF1 alpha and inhibition of platelet aggregation in vivo by the administration of glandular kallikrein.
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PMID:Effects of orally administered glandular kallikrein on urinary kallikrein and prostaglandin excretion, plasma immunoreactive prostanoids and platelet aggregation in essential hypertension. 388 84

Urinary kallikrein excretion (UKal), determined by the esterase method, was measured in 10 normotensive volunteers, 10 patients with essential hypertension and in 7 patients with primary aldosteronism before and after operative removal of the adenoma. UKal values were low in 5 of the patients with essential hypertension. Preoperative UKal values in the patients with aldosteronism did not differ significantly from those of the normal subjects, but decreased in all after operation in parallel with changes in urinary excretion of tetrahydroaldosterone and plasma aldosterone concentration. The study supports the assumption of an association between the renal kallikrein-kinin system and the mineralocorticoid state in man.
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PMID:Urinary excretion of kallikrein before and after operation for aldosterone-producing adenoma. 389 26

The kallikrein-kininogen-kinin system has been postulated to play a role in the regulation of blood pressure and modulation of renal salt and water transport. The activity of this system has usually been determined by measurements of urinary kallikrein excretion. However, urinary kallikrein rarely correlates with simultaneously measured urinary kinins. To further evaluate the factors influencing urinary kinin excretion, we evaluated the role of urinary kininogen in this system. Urines were analyzed from normal subjects and individuals with untreated essential hypertension and end-stage renal disease. Intact urinary kininogen was significantly correlated with urinary kinins in normal subjects (r = 0.65, P = 0.003) and essential hypertensives (r = 0.52, P = 0.026). In both essential hypertension and end-stage renal disease, urinary kinins were significantly decreased (8.00 +/- 1.93, 0.90 +/- 0.18, P less than 0.05, respectively) compared to controls (23.73 +/- 5.20). In essential hypertensives, the reduction in urinary kinins was paralleled by a reduction in intact kininogen with a normal excretion of kallikrein. In end-stage renal disease, the reduction in kinins was paralleled by a reduction in kallikrein with a normal excretion of intact kininogen. This data suggests that kininogen may be an important determinant of urinary kinin excretion in various disease states.
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PMID:The role of urinary kininogen in the regulation of kinin generation. 391 Sep 18

Urinary kallikrein excretion was evaluated in 85 normal subjects and in 149 uncomplicated and recently diagnosed essential hypertensive patients. Moreover, the possible interrelationships between urinary kallikrein excretion and age, sex, electrolyte excretion, and plasma renin activity were examined. In patients with essential hypertension, urinary kallikrein excretion was similar to that of normal subjects. In these patients the enzyme was weakly and positively related to urinary potassium and plasma renin activity; no correlation was found with blood pressure, urinary sodium, age, or sex. In normal subjects and in patients with essential hypertension, the variables studied account for only 25% and 17%, respectively, of the variability of urinary kallikrein excretion. We conclude that the relatively short duration of hypertension in our patients may explain the unaltered values of urinary kallikrein excretion with respect to controls.
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PMID:Urinary kallikrein activity is not altered in human essential hypertension. 391 22

The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KC1/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2 +/- 3.5/99.6 +/- 1.9 mm Hg to 137.4 +/- 2.9/89.1 +/- 1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.
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PMID:Hemodynamic, renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: long-term antihypertensive effect of potassium supplementation in essential hypertension. 392 52

In twenty-five outpatients with essential hypertension, the relevance of renal kallikrein excretion for inter-individual differences in the blood pressure response to changes in dietary sodium intake was investigated. The patients were studied during 2 weeks of high (300 mmol) and 2 weeks of low (50-100 mmol) sodium intake. In addition there were two control periods of normal sodium intake, one lasting 4 weeks at the beginning and one lasting 2 weeks at the end of the study. Blood pressure, body weight and 24 h urinary sodium and kallikrein excretion were measured at the end of all periods. At the end of the first control period, 1 mg furosemide per kg body weight was administered intravenously, and the urinary excretion of kallikrein and sodium were measured 30 and 120 min later. The difference in mean arterial pressure (delta MAP) between high and low sodium intake ranged from + 18 to -8 mmHg. The eight patients with a delta MAP greater than 10 mmHg were regarded as salt-sensitive. They were older and had a higher initial blood pressure than salt-insensitive patients. For all patients, urinary kallikrein excretion at the end of the low sodium period (123(SEM 20.3) micrograms 24 h-1) was significantly higher than at the end of the first control period (96(SEM 16.3) micrograms 24 h-1, P less than 0.01) and at the end of the high sodium period (96(SEM 23.7) micrograms 24(-1), P less than 0.01). When compared with salt-insensitive patients, salt-sensitives had lower levels of urinary kallikrein excretion and a blunted kallikrein response to dietary sodium restriction and furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is the renal kallikrein system relevant to sodium sensitivity in patients with essential hypertension. 392 10


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