Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To further clarify the role of the renal kallikrein-kinin system in essential hypertension, a sensitive and simple method for the determination of both human urinary kininase I and kininase II was established, and the system components were determined in patients. In the measurement of kininase activity, desalted urine samples were incubated with synthetic bradykinin, and the reaction was terminated with kininase inhibitors, ethylene diamine tetraacetic acid and phenanthroline. Thus, kininase activity was determined as the kinin-destroying capacity. Moreover, the specific inhibitor for kininase II, SQ14225, was applied for the separation of kininase I and kininase II activities. Daily urinary excretions of total kininase and kininase I activities were significantly higher in essential hypertensive patients than those in normotensive subjects, whereas no difference was observed in kininase II activity. As reported previously, daily excretions of urinary kallikrein and kinin simultaneously determined in these patients were significantly lower than excretions in normotensive subjects. From these results, it was suggested that not only decreased renal kallikrein, but also increased kininase activity, may play an important role in the suppression of the renal kallikrein-kinin system through the reduction of active kinin level in essential hypertension.
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PMID:Urinary excretions of kininase I and kininase II activities in essential hypertension. A sensitive and simple method for its kinin-destroying capacity. 301 73

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comprehensive studies on the renal kallikrein-kinin system in essential hypertension. 302 78

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily excretions of urinary kallikrein (KAL) quantity and activity, kinin (KIN), total and pre-KAL, and kininase I and II were measured in 21 normotensives (NT), 29 patients with NRH and 16 patients with LRH. The daily excretions of both KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in NRH and LRH than in NT. That of kininase I was significantly higher in NRH and LRH than in NT, but that of kininase II was not. In comparing NRH and LRH, the urinary excretions of KAL activity and KIN were lower in LRH than in NRH, and that of kininase I was higher in LRH than in NRH. The KAL/total KAL ratio did not show any significant difference among NT, NRH and LRH. These findings suggest that the suppression of the renal K-K system in EHT seems to be due to both the decrease of KAL through the pre-KAL synthesis in the kidney and an increase of kininase I activity, but not to the inhibition of conversion from pre-KAL to active KAL and the more obvious suppression of this system in LRH than in NRH may be partly explained by KAL inhibitors and/or increased kininase I activity.
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PMID:Study on the renal kallikrein-kinin system in normal and low renin subgroups of essential hypertension. 610 Jul 42

Bradykinin (BK) and [des-Arg9]-bradykinin (-9BK) concentrations in blood and urine samples from 18 normotensive subjects and 23 patients with low-renin essential hypertension were determined by radioimmunoassay. BK and -9BK levels in venous blood from normotensive subjects were 67.1 +/- 60.8 pg/ml and 204.1 +/- 44.5 (mean +/- S.D.), respectively, and levels in urine from normotensive subjects were 5.3 +/- 5.3 ng/ml and 1.6 +/- 1.2, respectively. The blood and urinary levels of BK and -9BK in low-renin essential hypertensives were not significantly different from those of normotensives and did not change when the hypertensives were treated with the new orally active angiotensin I-converting enzyme (ACE) inhibitor, enalapril (MK421). It has been proposed that BK levels do not change with ACE inhibition because under these conditions BK might be metabolized to -9BK by kininase I. Since -9BK levels did not increase with MK421 treatment, this possibility can be excluded. The absence of elevations in blood and urine BK and -9BK after administration of MK421 does not support an involvement of kinins in the mechanism of antihypertensive action of MK421 in these patients. On the basis of the data, it is not possible to exclude such an involvement, however, because local changes in kinin concentrations could occur that are not reflected by changes in circulating or urinary kinin levels.
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PMID:Immunoreactive bradykinin and [des-Arg9]-bradykinin in low-renin essential hypertension--before and after treatment with enalapril (MK 421). 631 33