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

To study the urinary kallikrein excretion before the delivery of term pregnancy we measured its excretion preterm (between 32-36 gestational week) in 13 patients with normotensive pregnancy and 17 patients with pregnancy-induced hypertension and one to five days before the delivery at term in 18 and 22 patients, respectively. In normotensive pregnancy urinary kallikrein excretion remained unchanged during the late third trimester until delivery (12.6 +/- 1.7 ncat in 24 hours in preterm, 10.8 +/- 1.2 before delivery). In pregnancy-induced hypertension and particularly in pre-eclampsia urinary kallikrein excretion was lower than in normotensive pregnancy and the decrease became more marked as the time of delivery approached (respective values: in pregnancy induced hypertension 9.2 +/- 1.2 and 7.0 +/- 0.7; in pre-eclampsia 7.6 +/- 1.3 and 7.3 +/- 0.9). The decrease in urinary kallikrein excretion suggests progressive disturbances in the interactions of renal vasoactive systems (the kallikrein-kinin system, the renin-angiotensin system and prostaglandins) with resultant changes in renal hemodynamics.
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PMID:Urinary kallikrein excretion in normal and hypertensive pregnancy at term. 364 2

Urinary kallikrein activity, intake, and excretion of sodium and water were measured in metabolic balance studies on spontaneously hypertensive rats (SHR) of the Okamoto-Aoki strain and normotensive Wistar-Kyoto rats (WKY) on a normal sodium diet from 4 through 15 wk of age. Urinary excretion of active and total kallikrein was significantly lower in SHR at all ages examined and represented a stable percentage of the values in age-matched WKY throughout development, on the average 69.5 and 67.4%, respectively. SHR exhibited a lower urinary excretion of sodium and water than WKY, a higher cumulative sodium balance at all ages studied, and a higher cumulative water balance only at ages 7 and 8 wk. The slopes of the regression lines correlating urinary kallikrein to systolic arterial pressure and to urinary excretion and cumulative balance of sodium and water were always significantly less in SHR than in WKY. The results of the present study indicate that SHR developing hypertension exhibit a precocious and stable abnormality in renal excretion of kallikrein activity.
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PMID:Reduced urinary kallikrein activity in rats developing spontaneous hypertension. 364 33

Fawn-hooded (FH) rats, primarily males, develop spontaneous low-renin hypertension associated with reduced urinary excretion of kallikrein as early as 2 months of age, followed by progressive glomerular sclerosis and proteinuria as early as 3 months of age. In the present study we determined the effects of early (5-7 weeks) or late (5 months) orchiectomy on the blood pressure and nephropathy of FH rats, compared to sham-operated (control) FH males. Early orchiectomy reduced significantly the progression of glomerular sclerosis and of proteinuria and ameliorated the hypertension but had no significant effect on excretion of urinary kallikrein. Late orchiectomy, in contrast, had no significant effect on the progression of glomerular sclerosis or proteinuria but did significantly reduce the blood pressure and marginally increase the excretion of urine kallikrein. These results suggest that (a) male sex hormones may play a role in the pathogenesis of hypertension and nephropathy in the FH rats and (b) renal disease in this strain progresses in spite of improvement in blood pressure.
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PMID:Contrasting effects of early and late orchiectomy on hypertension and renal disease in fawn-hooded rats. 365 Jun 58

Hypertension occurs more frequently in U.S. blacks than whites and is more severe. Blacks represent a disproportionate percentage of patients receiving dialysis treatment. This disproportion raises the question of whether the renal circulation of blacks is more sensitive to the damaging effects of elevated intraarterial pressure or whether it is structurally different in ways that would render it more prone to damage. The first part of the question has not been conclusively answered although some data support the hypothesis. For the second part, it is clear that malignant nephrosclerosis of blacks is different from that of whites in an absence of fibrinoid necrosis of arterioles and glomeruli and the presence of musculomucoid intimal hyperplasia of small arteries. Whether this is a genetically determined reaction to damage has not been determined. It is a widely held belief that the kidney is the cause of much essential hypertension. In fact 6 cases of essential hypertension in blacks have been "cured" by renal transplantation, strongly supporting the belief. Also blacks differ from whites in 2 ways that could be relevant for their increased prevalence of hypertension: they excrete sodium loads more slowly and have a markedly lower urinary kallikrein. The former could be responsible for the predominance of salt-dependent hypertension in blacks and the latter could reflect a racial deficiency in a naturally occurring vasodilator system.
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PMID:Systemic hypertension and the kidney in black patients. 368 9

Kallikrein and kininase activities were determined in urine of 58 hospitalized pregnant patients: 15 with E.P.H. gestosis, 10 with chronic hypertension, 18 with non proteinuric pregnancy induced hypertension, 15 with no hemodynamic disease as controls. All our cases with hypertension were treated with alpha-methyl-dopa. A significant increase in urinary kininase activity was shown by only E.P.H. gestosis group vs. controls. In the same group we found a significant decrease in urinary kallikrein activity vs. controls, in contrast with the results obtained previously, perhaps because of the different measuring method. The kininase/kallikrein ratio, theoretically indicative of kinins activity, increased significantly only in the E.P.H. gestosis group.
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PMID:Urinary kallikrein and kininase activity in normal and complicated by hypertension pregnancy. 381 2

The renal kallikrein-kinin system is thought to participate in blood pressure regulation and displays abnormalities in human hypertension, as well as in many animal models of hypertension. Urinary excretion and tissue levels of renal kallikrein were measured in streptozocin (STZ)-diabetic rats in relation to blood pressure, glycemia, and insulin treatment. In study 1, STZ-diabetic rats with marked hyperglycemia showed reduced kallikrein-like esterase excretion, compared with control rats, when first measured after 7 days of diabetes (9.9 +/- 2.5 versus 17.5 +/- 2.4 EU/24 h, P less than 0.05). This difference increased with time and, after 210 days, urinary esterase excretion in diabetic and control rats was 6.7 +/- 2.1 and 39.0 +/- 6.0 EU/24 h, respectively (P less than 0.001). Urine kallikrein, measured by radioimmunoassay, was similarly reduced in diabetic rats (40.4 +/- 8.0 versus 88.0 +/- 6.5 micrograms/24 h, at 30 days, P less than 0.001). At 120 days, systolic blood pressures were elevated in diabetic rats (P less than 0.05), and at 180 days over 60% of the diabetic rats had pressures above the highest pressures of control rats. In study 2, STZ-diabetic rats were treated with insulin for 2 wk (2 U NPH at 0800 h, or 2 U NPH at 0800 and 1600 h). In the single-dose group, with hyperglycemia similar to that of diabetic rats in study 1, kallikrein excretion was reduced as early as day 2, compared with nondiabetic rats (56.0 +/- 6.1 versus 109 +/- 9.4 micrograms/24 h, respectively, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary and renal tissue kallikrein in the streptozocin-diabetic rat. 384 6

Whether to determine the urinary kallikrein (UKK) levels in the second trimester of pregnancy is valuable in predicting of gestosis, especially of hypertension, was studied using samples of urine obtained from 500 cases of pregnant women without gestosis, 50 pregnant women with gestosis and 50 cases of pregnancy with a variety of complications other than gestosis. The main results obtained were as follows: In normal pregnancy, UKK levels elevated with pregnancy for a peak in the first to the second trimester of pregnancy, tapering off thereafter. The UKK level was significantly lower in 20 pregnant women with gestosis especially in hypertensive type than in pregnant women without gestosis (p less than 0.001). Pregnant women with normal blood pressure who suffered no gestosis and had an extremely low UKK level, accounted for 9.8% of all pregnant women studied. This figure includes a large number of those who were in a high risk group for the onset of gestosis. From these findings, UKK was considered to be useful as one of the factors used in predicting the onset of hypertension in association with gestosis and we are now studying pregnant women in the 20th and 30th week of pregnancy in more detail.
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PMID:[Urinary kallikrein levels during pregnancy]. 384 54

A series of acetyl-peptidyl-amides containing the amino acid sequence around the Arg-Ser kallikrein cleavage site of bovine kininogen were synthesized and tested for their ability to inhibit both the kinin-releasing activity and the amidase activity of purified human urinary kallikrein. The substrate analogues were competitive inhibitors for human urinary kallikrein and the heptapeptides (P4-P3'), hexapeptides (P3-P3'), and pentapeptides (P2-P3') gave Ki values of 140, 64, and 18 microM respectively, while the tetrapeptides (P1-P3'), tripeptides (P1'-P3') and dipeptides (P2'-P3') had little or no inhibitory activity. The effective analogues had neither kinin-like nor kinin-blocking activity on the rat uterus either before or after exposure to human urinary kallikrein. The effective human urinary kallikrein inhibitors were further examined for their effect on other serine proteases, including human plasma kallikrein, plasmin, complement components (C1s, C1r), bovine coagulation factors (IIa, IXa, and Xa), elastase, and trypsin. These peptides showed little inhibition of the circulating serine proteases but yielded a Ki for the nonspecific protease trypsin in the microM range. These results should provide the basis for the development of highly specific tissue kallikrein inhibitors to aid in elucidating the in vivo role(s) of tissue kallikreins.
Hypertension
PMID:Specificity of substrate analogue inhibitors of human urinary kallikrein. 384 67

Decreased urinary kallikrein (UK) output has been suggested as a preclinical indicator of essential hypertension. In preparation for UK studies in hypertension prone Utah kindreds, we assessed selected UK assay parameters and physiological variability. Precision for the colorimetric kallikrein assay was quite acceptable, coefficient of variation (CV) less than 5% within run and 14% day-to-day at a concentration of 9.5 TU/l. The mean recovery was 105% and assay results were correlated with results from the 3H-TAME esterase method, r = 0.990. Urine specimens were stable at room temperature for up to 4 days, frozen at -20 degrees C for 6 weeks, or frozen at -80 degrees C after Sephadex treatment for a year. UK output varied significantly throughout the day with excretion highest in the morning. Urine collections at 10.00, 12.00 and 14.00 had significantly (p less than 0.05) more UK than the overnight collection. Intra- and inter-individual variations were of the same magnitude, mean 20%. In children UK output increased with age until the adult levels were reached at age 15. Male and female values were similar. Smoking; consumption of alcohol, coffee, tea, cola of chocolate; and female hormone medications did not significantly influence the 12-hour UK output in the 1110 caucasian subjects.
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PMID:Urinary kallikrein: assay validation and physiological variability. 385 8

Monoclonal antibodies to purified human urinary kallikrein have been developed. Selection of antibody producing clones was based on 125I-kallikrein binding activity of hybridoma media in both radioimmunoassay and enzyme-linked immunosorbent assay. Three clones (2 IgG1, 1 IgG2b) were subcloned, characterized, and compared with the polyclonal antiserum generated in rabbits immunized with the purified kallikrein. With radioimmunoassay, mouse ascitic fluids or rabbit antisera dilutions showing 50% binding to 125I-kallikrein were 1:1.2 X 10(6) (E7A9), 1:1.2 X 10(5) (H6A6), 1:8.0 X 10(4) (E12H1), and 1:1.4 X 10(6) (the rabbit antisera). With enzyme-linked immunosorbent assay, mouse ascitic fluids from clones E7A9 and H6A6 showed half-maximal absorbance at dilutions of 1:2.1 X 10(5) and 1:1.0 X 10(5) respectively, and the polyclonal antiserum showed half-maximal absorbance at a dilution of 1:2.0 X 10(4). These monoclonal antibodies showed no cross-reactivity with rat tissue kallikrein, rat urinary plasminogen activator, or dog pancreatic kallikrein, while the polyclonal antiserum showed some cross-reactivity. The binding of monoclonal or polyclonal antibodies to 125I-human urinary kallikrein was not affected by human plasma kallikrein, thrombin, or urokinase in a competitive radioimmunoassay. By using purified human urinary kallikrein immobilized to agarose, antibodies produced by clones E7A9 and H6A6 and in the rabbit antisera were purified to homogeneity. Each of these affinity-purified antibodies inhibited the esterase activity, and two of the three inhibited the kininogenase activity, of human urinary kallikrein. A sandwich immunosorbent assay was developed to measure this kallikrein using monoclonal antibody from the clone E7A9 in conjunction with the polyclonal antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Characterization of monoclonal and polyclonal antibodies to human tissue kallikrein. 385 80


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