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

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.
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PMID:Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism. 66 67

Previous studies in a population of 721 children aged 2--14 years demonstrated the familial aggregation of blood pressure in children, and a significant regression coefficient (b = 0.25) of follow-up on initial blood pressures over a four-year period. Urinary kallikrein concentration (UKal) also aggregated in families, was lower in black than in white children and was inversely related to blood pressure. Further studies in the same cohort have been conducted. These variables were again measured in 484 children in 129 families seven to eight years after the initial blood pressure and three to four years after the original UKal measurements were made. Familial aggregation again was found for blood pressure and urinary kallikrein. Blood pressure tracking was demonstrated by the finding that blood pressure scores at the third survey were related significantly to those at both previous surveys. Kallikrein concentrations in casual urines at Survey 3 were related to those obtained at Survey 2 (r = 0.499), and were again significantly lower in black than in white children (log = 3.84 +/- 0.8 vs 4.37 +/- 0.7; P less than 0.001). These were significant inverse relations between UKal/creatinine concentration and blood pressure in both white and black children. Thus, familial aggregation of blood pressure, blood pressure rank and concentration of kallikrein in casual urine specimes are relatively stable in children over an eight-year period of observation. This study demonstrates in a free living population of normal children, a stable relation between blood pressure and an enzyme which is involved in the production of potent vasodilator peptides and is related to hypertension in adults.
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PMID:Stability of blood pressure rank and urinary kallikrein concentration in childhood: an eight-year follow-up. 69 59

Many factors are to be considered in maintaining normal blood pressure. Authors study the behavior of urinary kallikrein (U.K.) and plasma dopamine-beta-hydroxylase (DBH) activity in various forms of hypertension. The values of U.K. excretion in normals were 20.5 +/- 1.8 E.U./24 h. In essential hypertensive patients (9.4 +/- 2.0 E.U./24 h) U.K. decreased, while in secondary hypertension it was significantly higher (33.8 +/- 3.0 E.U./24 h). Plasma DBH activity in essential hypertensive patients (17.72 +/- 2.33 I.U./ml) was similar to controls (20.22 +/- 1.39 I.U./ml); in secondary hypertension the mean values of plasma DBH were decreased (12.31 +/- 2.55 I.U./ml). No correlation between U.K. and plasma DBH activity was observed in normals and in various forms of hypertensive patients. U.K. seems a more reliable factor than plasma DBH in defining the different types of hypertension.
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PMID:Urinary kallikrein excretion and plasma DBH activity in hypertension. 74 55

We investigated the relationship of the kallikrein-kinin system and the renin-angiotensin system in the regulation of blood pressure, salt and water excretion, and renal blood flow. Normotensive and hypertensive black and white men were studied during unresticted sodium intake as well as on a 10-meq/day sodium intake; potassium intake was held constant throughout the study (80 meq/day). During unrestricted sodium intake, urinary kallikrein activity was greater in white normotensives than white hypertensives or black normotensives. There was no difference (P greater than 0.05) between white and black hypertensives or between black normotensives and black hypertensives. All groups had greater urinary kallikrein activity on low sodium vs. unrestricted sodium intake, but the increase in black hypertensives was small, and they excreted significantly less kallikrein than the ogher groups on the low sodium diet. Plasma renin activity showed similar increments after sodium restriction in all groups. Urinary kallikrein activity correlated with renal blood flow in all groups except the black normotensives on low sodium intake. Renal blood flow could be correlated uniformly with log (urinary kallikrein activity/supine plasma renin activity) in all groups on either diet. Urinary sodium and potassium excretion and urine volume were not different among the groups. We conclude: (a) important racial differences exist in urinary kallikrein activity that are unrelated to sodium or potassium excretion or urine volume; (b) dietary sodium restriction further delineates racial differences and suggests alternative pathophysiologic mechanisms for huma hypertension; (c) urinary kallikrein activity correlates with renal blood flow; and (d) our data support the concept that the kallikrein-kinin system and the renin-angiotensin system contribute to the regulation of renal blood flow and may account for racial differences in renal vascular resistance.
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PMID:Urinary kallikrein and plasma renin activity as determinants of renal blood flow. The influence of race and dietary sodium intake. 87 78

Plasma, blood, and urine volumes, renal kallikrein, and arterial pressure were measured in control and renal hypertensive rats in order to study the role of the renal kallikrein system in regulating arterial pressure and its relation with the alterations in water handling observed in hypertension. A decrease in kallikrein content of the kidney (157 +/- 17 versus 236 +/- 16 ng bradykinin equivalents per gram of tissue in control rats) was associated with an increase in plasma volume (38.0 "/- 1.6 versus 32.0 +/- 0.9 ml/kg body weight in control rats) and an increase in urine volume (45.5 +/- 4.9 versus 20.3 +/- 1.6 ml/kg body weight per 24 hours in control rats). No linear correlation was found between these factors and the arterial pressure of hypertensive animals. These findings support the hypothesis that changes in renal kallikrein are more directly related to water and electrolyte metabolism than to the arterial pressure regulation. Our results also suggest an interaction between the kallikrein-kinin and the renin-angiotensin-aldosterone systems. The possible relations of both enzymatic systems to the regulation of arterial pressure and of water-electrolyte handling are summarized schematically.
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PMID:Renal kallikrein system, volemia, and renal hypertension. 87 70

Urinary kallikrein excretion was studied in rats bred for susceptibility and resistance to the hypertensive effect of salt. The rats were on a regular rat chow diet (0.45% sodium content) and tap water and were not hypertensive at the time of the study. Urinary kallikrein excretion, measured by kinin radioimmunoassay, was 10 to 20 times lower in the susceptible rats than in the resistant rats (4.39 +/- 1.61 microgram/24 hours and 56.4 +/- 5.8 microgram/24 hours, respectively; P less than 0.001). Urinary kallikrein excretion was also measured in New Zealand genetically hypertensive rats and in normotensive Wistar-Otago rats (controls). Kallikrein was found to be significantly lower in the genetically hypertensive rats than in the controls (49.1 +/- 6.2 microgram/24 hours and 76.8 +/- 6.9 microgram/24 hours, respectively); however, when expressed per 100 g of body weight, there was no significant difference. In conclusion, although urinary kallikrein excretion per rat was decreased in the genetically hypertensive rats when compared with the controls, this difference could be caused by the lower body weight of the genetically hypertensive rats. Urinary kallikrein excretion, when expressed per 100 g of body weight, is significantly lower in susceptible than in resistant rats. This could be a consequence of a genetic defect that may play a role in the development of hypertension, perhaps through alteration of renal function.
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PMID:Urinary kallikrein in rats bred for susceptibility and resistance to the hypertensive effect of salt and in New Zealand genetically hypertensive rats. 87 72

Urinary kallikrein was measured in normal pregnant women stages of gestation and in women who developed hypertension in late pregnancy. Mean urinary kallikrein was highest in the first trimester and fell significantly in the third trimester to nonpregnosterone system. A negative correlation was observed between urinary kallikrein and the length of gestation in normal pregnancy. Urinary kallikrein fell significantly below nonpregnant levels in patients with hypertension while the renal excretion of sodium and water was not different from that in normal pregnancy of the same dy is discussed in the light of factors known to increase kallikrein excretion. It is considered unlikely that this elevation is due to the escape from the sodium-retaining effect of the high aldosterone of pregnancy. It may be due in part to the stimulating effect of raised angiotensin II levels but it is considered most likely to be the effect of a circulating renal vasodilator. The reduced kallikrein in hypertension of pregnancy may play a part in the development of the hypertension and resembles the reduced kallikrein excretion in essential hypertension.
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PMID:Urinary kallikrein in normal and hypertensive pregnancies. 100 45

Urinary kallikrein excretion was measured in 21 healthy subjects and 44 patients with various types of hypertension. The kallikrein activity was determined by the method of esterolytic assay. The excretion rates in normal subjects were 112.9 +/- 11.1 (S.E.) EU/day. The kallikrein excretion was decreased in patients with essential hypertension, the mean estimated values were 75.2 +/- 10.0 EU/day. In this disease, however, an enhancement of urinary kallikrein was observed after sodium depletion. An obvious increase in kallikrein excretion was found in the primary aldosteronism. In primary aldosteronism and renovascular hypertension, one of the secondary aldosteronisms, there was a good correlation between the urinary kallikrein output and the urinary sodium excretion. The present data indicate that the renal kallikrein-kinin system, one of the renal antihypertensive factors, is suppressed in essential hypertension and is under the influence of mineralocorticoid levels.
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PMID:Urinary kallikrein excretion and sodium metabolism in hypertensive patients. 118 19

Urinary kallikrein excretion is reduced in patients with hypertension of unknown etiology. In addition, the excretion of this renal, kinin-forming enzyme was found to be elevated in hypertensive patients with primary aldosteronism. Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. The relationship between kallikrein excretion and aldosterone activity may directly reflect the intrarenal activity of the kallikrein-kinin system, as determined by studies of kallikrein levels from isolated renal cells or of plasma kinin levels in man in response to postural changes or saline loads. Some patients with essential hypertension do not show a normal increase in kallikrein excretion in response to low dietary sodium intake despite an apparently normal aldosterone response, suggesting that there may be a defect in the renal kallikrein-kinin system in these patients. Whether these findings are of pathogenetic significance in human hypertensive disease remains to be determined.
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PMID:Relationships among urinary kallikrein, mineralocorticoids and human hypertensive disease. 124 55

The pathogenesis of hypertension in autosomal-dominant polycystic kidney disease (ADPKD) is unclear, but increased activity of the renin-angiotension system may contribute. The renal and systemic hemodynamic response to lisinopril, an angiotension converting enzyme (ACE) inhibitor, in patients with ADPKD without renal failure was compared with the response in matched unaffected family members. Mean blood pressure and renal vascular resistance decreased in the affected group after lisinopril, with no significant change in the unaffected group. Glomerular filtration rate (GFR) was unchanged and therefore filtration fraction fell significantly. Changes in urinary excretion of 6-keto-PGF1 alpha and kallikrein suggested that increased renal synthesis of PGI2 or activation of the renal kallikrein-kinin system were not likely to be responsible for the hemodynamic effects. The acute decrease in renal vascular resistance without change in GFR suggests that ACE inhibition may have a particular value in the treatment of hypertension associated with ADPKD which should be assessed by further long-term studies.
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PMID:Effects of angiotensin converting enzyme inhibition in adult polycystic kidney disease. 131 77


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