Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effect of the duration and severity of hypertension on arterial wall metabolism 28 enzyme activities and several macromolecular complexes were histochemically studied in normotensive (WK), moderately (SHR) and strongly hypertensive (SP-SHR) rats at various ages. The results indicate that the abnormalities of 5' nucleotidase, acid esterase, cholinesterase and Alk.P. appeared in prehypertensive 4 w.old SHR. The posthypertensive changes, fluctuating in relation to the duration of hypertension, concerned: the pentose pathway, Krebs cycle and glycolosis -linked dehydrogenases; lysosomal enzymes; glycogen-phosphorylase and MAO; glycosaminoglycan and glycoprotein content. The structural and metabolic response presented several local and regional differences. The metabolic changes were greater in the aorta than in the caudal and femoral arteries. The comparison between SHR and SP-SHR indicates that the blood pressure (BP) at 170 mm Hg seems well tolerated during a long period of time. Severe lesions such as degeneration and failure of lipolytic activity in aortic smooth muscle cells (SMC), notable and early (8 mo.) in SP-SHR with 240 mm Hg were less intense and appeared later (13 mo.) in SHR with 190 mm Hg. The level of hypertension, rather than its duration, appears as a determining factor of posthypertensive vascular damage.
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PMID:Enzyme-histochemical changes in arteries of genetically hypertensive rats (SHR, SP-SHR). 632 44

The plasma renin activity (PRA), plasma volume (PV), urinary excretion of Kallikrein (UK) and PGE2, PGF2 alpha, 6-keto PGF1 alpha and TXB2 were measured in 24 ambulant patients without treatment on normal sodium diets with pregnancy-induced hypertension (HT) (diastolic BP greater than or equal to 90 mmHg, appearing after 20 weeks' pregnancy and absent 2 months after delivery). The UK was measured by an esterase technique, prostaglandins by radioimmunological assay and PV by dye dilution (Evans blue). Two subgroups of patients were identified according to the evolution of their blood pressure at rest at home; the first (7 patients) with labile HT, and the second (14 patients) with permanent HT. The PRA was significantly lower (p less than 0,001) in patients with permanent compared to labile hypertension (4,7 +/- 0,3 compared to 12,2 +/- 0,8 ng/ml/h) and compared to a control group of normotensive pregnant women (6,5 +/- 0,5). The PV, expressed as a percentage of the theoretical volume with respect to the stage of pregnancy and body surface area was low in both groups. In permanent HT: 1) there was no correlation between PV and PRA, 2) a positive correlation between UK and urinary 6-keto PGF1 alpha (r = 0,62; p less than 0,001) and PGE2 (r = -0,51, p less than 0,05). Discriminative linear analysis showed that urinary 6-keto PGF1 alpha was mainly related to PRA and to a lesser degree to UK.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renin-angiotensin-aldosterone system, blood volume, serum uric acid and urinary excretion of prostaglandins and kallikrein in the arterial hypertension induced by pregnancy]. 644 41

The authors evaluated 500 patients who yielded urine specimens containing red and white blood cells but that gave negative reagent test strip reactions to determine the medical usefulness of the microscopic examination in such cases. Half of the patients had a history of, or current signs and symptoms of genitourinary or renal disease (GURD), or had indwelling catheters, hypertension, or diabetes. The other half did not display these conditions. Red blood cells occurred rarely, and no red blood cell associated GURD was detected in these patients. Five had lower urinary tract infection. Seventy-two underwent further workup, but no GURD was found. Physicians did not comment or take action on the report in other patients. The authors found the test for leukocyte esterase and nitrite (LN) to have a predictive value for a negative result of 97% for exclusion of bacteruria. Based on these observations, the authors established in 1982 a policy that microscopic examination would be performed only on specimens negative by reagent test strip (including LN) if a "diagnostic urinalysis" (DU) was ordered. The authors recommended that DU be requested only for patients suspected of GURD. This has eliminated microscopic examinations on 25% of specimens and reduced costs.
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PMID:Usefulness of microscopic examination in urinalysis. 654 7

Estimations of prekallikrein and kallikrein inhibitor by means of TAME-esterase method and of the content of kininogen by biological procedure were carried out in blood plasma, isolated from right and left ventricles of heart, of rats with spontaneous hypertension, Okamoto-Aoki strain, and of the normotensive animals Wistar-Kyoto strain. The animals were 2=3 months, 6=8 months and 12=14 months old. Development of spontaneous hypertension was accompanied by an increase in the kallikrein-kinin system components studied. Content of prekallikrein and kininogen was higher in blood plasma from left heart ventricle than in blood from right ventricle, independently of the age of the rats, by 6=10% and 33=40%, respectively. Lung tissue was shown to carry out a definite reserve function in the compensatory increase of the kallikrein-kinin system potential under conditions of spontaneous hypertension.
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PMID:[State of the kallikrein-kinin system in blood from the heart ventricle in the dynamics of spontaneous hypertension in the rat]. 657 Mar 84

The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation has been assessed by measurement of urinary kallikrein activity in 41 renal transplant recipients. The urinary tosyl arginine methyl esterase assay was used. The urinary kallikrein in these patients appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertension (mean blood pressure 156 +/- 3/98 +/- 2 mm Hg) and excreted less kallikrein (4.0 +/- 1.2 versus 12.5 +/- 4.0 esterase units [EU] per 24 hours, p less than 0.05) than their 18 normotensive counterparts (mean blood pressure 132 +/- 2/77 +/- 1 mm Hg, both p less than 0.01). Subjects with renal complications of transplantation (acute tubular necrosis [ATN], nine patients, or acute rejection [AR], eight patients) also excreted less kallikrein than the 28 subjects without such complications (3.4 +/- 0.9 versus 10.3 +/- 2.7 EU/24 hours, p less than 0.02). Among those with acute renal complications, subjects with ATN excreted less kallikrein than those with AR (1.3 +/- 0.3 versus 5.7 +/- 1.7 EU/24 hours, p less than 0.02). Cadaver graft recipients excreted less kallikrein than living related donor graft recipients (2.1 +/- 0.4 versus 13.0 +/- 3.5 EU/24 hours, p less than 0.01), perhaps reflecting their higher blood pressures (mean systolic pressure 151 +/- 3 versus 140 +/- 3 mm Hg, p less than 0.04), relatively impaired renal function (creatinine clearance values 42 +/- 8 versus 62 +/- 5 ml/min, p less than 0.04), and higher incidence of ATN (nine cases versus none). The kallikrein-kinin system may be involved in the pathogenesis of hypertension and some forms of renal dysfunction after renal transplantation.
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PMID:Urinary kallikrein excretion after renal transplantation: relationship to hypertension, graft source, and renal function. 675 Oct 83

Iodine-labeled ([125I]) rat urinary kallikrein and rat urinary TAME esterase A2 were used as probes to look for urinary and plasma proteins that bind to these enzymes. Such proteins are presumptive enzyme inhibitors. Complexes formed with labeled enzymes were identified by polyacrylamide gel electrophoresis followed by autoradiography. Urine from young (6 weeks old) Dahl salt-sensitive (S) rats showed no, or only traces, of protein binding to kallikrein. Concomitant with the slow development of hypertension and proteinuria in S rats fed normal rat chow, one of the six kallikrein-binding proteins demonstrable in plasma was readily found in S-rat urine. This kallikrein-binding protein was called "KBP-1." R rats showed either no or much less KBP-1 in the urine, compared to S rats up to 5 months of age. A partly purified preparation of KBP-1 was shown to inhibit the TAME esterase activity of rat urinary kallikrein in the radiometric TAME assay. Urine of proteinuric S rats also contained two TAME esterase-binding proteins, TEBP-1 and TEBP-2, detected with the [125I]-esterase A2 probe. As S rats aged from 3 to 8 months, free KBP-1 disappeared from the urine in spite of increased and marked proteinuria and the continued presence of KBP-1 in plasma. Concomitant with this age-related loss of urinary KBP-1 there was a marked shift in S urinary proteins binding to [125I]-esterase A2 from TEBP-1 to TEBP-2. It was speculated that KBP-1 and TEBP-1 were the same protein detectable with either labeled kallikrein or labeled esterase A2. The concomitant disappearance of free KBP-1 (TEBP-1) and the appearance of free TEBP-2 in the urine of old, hypertensive, proteinuric S rats suggests that: 1) most of the KBP-1 (TEBP-1) is bound to enzyme(s) in old rats; or 2) KBP-1 (TEBP-1) is largely converted to TEBP-2 in old rats; or 3) both are true and that binding of KBP-1 (TEBP-1) to enzymes is associated with the generation of TEBP-2.
Hypertension
PMID:Proteins binding to kallikrein and esterase A2 in the urine of salt-sensitive and salt-resistant rats. 675 95

S and R female rats were raised on a 1% NaCl diet, and excretion rates of urinary protein, kallikrein esterase activity, and PGE2 were measured (1) at 1 1/2 months of age, when both S and R rats were normotensive, (2) at 3 months of age, when S rats were mildly hypertensive and R controls remained normotensive, and (3) at 6 months of age, when S rats were markedly hypertensive relative to the still normotensive R rats. Urinary protein excretion rate in S compared to R rats was slightly elevated at 1 1/2 months of age and greatly elevated at 3 and 6 months of age. Urinary kallikrein was measured by hydrolysis of TAME after separation of kallikrein from nonkallikrein TAME esterases on DEAE-Sephadex minicolumns. Kallikrein TAME esterase activity was the same in 1 1/2-month-old S and R rats but became reduced in S relative to R rats at 3 and 6 months of age, concomitant with the development of hypertension and marked proteinuria. Urinary PGE2 was decreased in S rats as compared to R rats at all ages, and therefore the strain difference in urinary PGE2 preceded the development of strain differences in blood pressure and urinary kallikrein activity. We conclude that (1) reduced excretion of urinary kallikrein TAME esterase activity in S rats is probably secondary to hypertension and severe proteinuria and (2) decreased urinary PGE2 excretion in prehypertensive S rats is compatible with, but does not prove, the presence of a primary defect in intrarenal PGE2 production that could be involved in initiating hypertension.
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PMID:Developmental patterns of blood pressure and urinary protein, kallikrein, and prostaglandin E2 in Dahl salt-hypertension-susceptible rats. 691 75

The relationships between urinary kallikrein (Ukal), and plasma renin activity (PRA), urinary aldosterone (Ualdo), Na+ balance, SK+, and renal function were studied in essential hypertensives (EHT) and normals. Ukal was measured by a radiochemical esterolytic assay. We studied 18 white patients with EHT (15 men, 3 women) ages 31.6 to +/- 2.1 (SEM) yrs, BP 138 +/- 2/95 +/- 2 mm Hg. and 12 white normals (NLS) (7 men, 5 women) ages 30.2 +/- 2.3 yrs, BP 112 +/- 4/71 +/- 2 mm Hg. All received a 5-day diet of 400 mEq Na+, 80 mEq K+/day, and 5 days of 10 mEq Na+, 80 mEq K+/day. All achieved Na+ balance by Day 5. On Day 5 of the low Na+ diet, 24 hr. Ukal in EHT was 15.8 +/- 2.4 (esterase units/24 hr) vs NLS, 17.0 +/- 2.8 PRA was the same in EHT and NLS, but Ualdo was higher in NLS. (Day 5, low Na+, EHT, Ualdo = 29.4 +/0 3.3 microgram/24h. vs NLS 41.8 +/- 4.7, p less than 0.02). Analysis of individuals showed that all NLS increased Ukal after salt restriction, while 3 EHT decreased Ukal after salt restriction. This abnormal response in EHT was not related to abnormalities in Ualdo, PRA, Na+ balance, SK+, or creatinine clearance. In 3 EHT with low-renin EHT, the Ukal response was normal. In two of four patients with primary aldosteronism, Ukal was normal despite increased Ualdo. The Ukal response to salt restriction is abnormal in some EHT, unrelated to Ualdo or PRA, suggesting either a primary defect in Ukal and/or the presence of other factors modulating Ukal in EHT.
Hypertension
PMID:Abnormal urinary kallikrein in hypertension is not related to aldosterone or plasma renin activity. 700 36

Urinary enzymes that hydrolyze the artificial substrate alpha-N-p-tosyl-L-arginine methyl ester (TAME) were studied in Dahl salt-sensitive (S) and salt-resistant (R) rats. Total urinary TAME esterase activity (kallikrein and non-kallikrein) showed a marked increase with dialysis against water, but only in hypertensive S rats with proteinuria. This phenomenon suggests the presence of dialyzable TAME esterase inhibitor(s) in urine following renal damage, but these data do not define what urinary esterases might be affected. Partially purified urinary kallikrein exhibited a ratio of kininogenase to esterase activity which was equal for S and R rats. Thus, the marked discrepancy between kininogenase and esterase activities reported by Carretero et al. with S and R whole urine is not a function of the S and R kallikrein molecules but is probably related to interfering substances in the whole urine. Urinary kallikrein excretion was measured on individual rat samples by TAME esterase activity following dialysis and separation from non-kallikrein TAME esterase(s) using DEAE-Sephadex minicolumns. S rats had lower urinary kallikrein excretion that R when the S rats were hypertensive and showed marked proteinuria. Young S and R rats raised on low salt showed similar blood pressures and similar kallikrein excretion. High salt (8% NaCl) diet decreased kallikrein excretion in both S and R, but the decrease was greater in the S rats which became hypertensive and had increased urine protein excretion. These data suggest that the lower urinary kallikrein excretion in S rats relative to R rats is probably a consequence of hypertension and renal damage rather than a primary cause of hypertension.
Hypertension
PMID:Total and kallikrein arginine esterase activities in the urine of salt-hypertensive susceptible and resistant rats. 700 38

Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17alpha-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1+/-0.4 vs. 4.8+/-0.5 esterase units (EU)/24 h, mean+/-SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2+/-2.3 vs. 11.7+/-1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance >/=80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3+/-0.3 vs. 5.4+/-0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9+/-1.2 vs. 8.4+/-0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8+/-78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6+/-2.0 for 24 black patients and 4.2+/-0.7 EU/24 h with creatinine clearance of 67.0+/-3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3+/-2.7 [n = 9], NREH = 11.7+/-1.8 [n = 10], LREH = 10.9+/-1.5 [n = 12]; white normals = 21.2+/-2.9 [n = 11], essential hypertension = 20.9+/-3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+/-2.4 [n = 10], NREH = 10.1+/-2.7 [n = 10], LREH = 7.4+/-1.1 [n = 13]; white normals = 19.1+/-2.7 [n = 13], essential hypertension = 17.5+/-2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+/-2.7 vs. 33.3+/-6.4 mug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17alpha-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essentil hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.
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PMID:Urinary kallikrein excretion in essential and mineralocorticoid hypertension. 735 84


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