Kallikrein-like activity in the urine of renal hypertensive rats

Croxatto, H.; Martin, Marisa

doi:10.1007/bf01897974

Cited by 59 publications

(24 citation statements)

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“…13 " 15 The present study is in agreement with these reports and extends these observations by demonstrating that rats with this type of renovascular hypertension have normal levels of immunoreactive glandular kallikrein in plasma. This finding indicates that if renal kallikrein plays a role in the pathogenesis of the hypertension, its contribution must be through a local mechanism in the kidney and not through a systemic effect, since immunoreactive glandular kallikrein in plasma did not change.…”

Section: Discussionsupporting

confidence: 92%

“…For example, urinary kallikrein excretion is diminished in renovascular hypertension, 13 "" and the subnormal production of this vasodilator system is thought to be involved in the pathogenesis of this type of hypertension. If urinary kallikrein excretion reflects the activity of the system in the peripheral circulation, changes in urinary kallikrein excretion should be expected to be paralleled by changes in the plasma concentration of immunoreactive glandular kallikrein.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we studied glandular kallikrein in the plasma and urine of rats in three different sets of experimental conditions: two-kidney, one clip hypertension; low sodium intake; and DOCA-salt hypertension. We chose these experimental conditions because urinary kallikrein excretion is below normal in two-kidney, one clip hypertension 13 " 15 but increases above normal in rats after either low sodium intake or DOCA-salt treatment.…”

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confidence: 99%

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Immunoreactive glandular kallikrein in plasma during alterations of urinary kallikrein excretion.

Rabito¹,

Scicli²,

Carretero³

1983

Hypertension

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SUMMARY To determine whether maneuvers known to modify immunoreactive urinary kallikrein excretion (iUKK) also alter the concentration of immunoreactive glandular kallikrein (iGKK) in plasma, we measured iGKK in the plasma and urine of rats before, at 1 week, and at 3 weeks after induction of two-kidney, one clip hypertension, low sodium intake, and DOCA-salt hypertension. Glandular kallikrein in plasma and urine was measured by radioimmunoassay. Clipping of a renal artery decreased iUKK from 11.7 ± 0.5 /xg/24 hr/100 g body weight (BW) to 7.8 ± 0.5 and 8.2 ± 0.5 at 1 and 3 weeks after surgery without significantly changing iGKK in plasma. The level of iGKK in the plasma did not correlate significantly with iUKK in the clipped group. Low sodium intake significantly increased iUKK, which rose from 6.6 ± 0.3 ngJ24 hr/100 g BW to 9.6 ± 0.5 and 13.9 ± 0.7 after 1 and 3 weeks. In addition, low sodium intake appeared to increase iGKK in plasma, and a significant positive correlation was observed between iUKK and iGKK in plasma in the group on low sodium diet (r = 0.65, p < 0.01). DOCA-salt treatment increased iUKK significantly from 10.4 ± 0.6 /ig/24 hr/100 gBW to 17.1 ± 1.4 and 22.6 ± 2.3 at land 3 weeks after. The iGKK in plasma increased from 13.8 ± 0.5 to 15.4 ± 0.7 ng/ml (p < 0.05) at 1 week after the DOCA-salt treatment began, but it returned to pretreatment levels 3 weeks later (14.5 ± 0.7 ng/ml, n.s.). There was no significant correlation between iUKK and iGKK in the plasma of the DOCA-salt-treated group. We conclude that the concentration of glandular kallikrein in plasma does not necessarily parallel changes in urinary kallikrein excretion, indicating that urinary kallikrein excretion cannot be taken as an indicator of the activity of the renal kallikrein-kinin system in the systemic circulation. sized by the kidney and excreted in the urine, catalyzes the formation of kinins, which are vasoactive peptides. The renal kallikrein-kinin system has been the focus of considerable attention because of its possible involvement in the regulation of renal function and in the pathogenesis of hypertension.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Immunoreactive glandular kallikrein in plasma during alterations of urinary kallikrein excretion.

Rabito¹,

Scicli²,

Carretero³

1983

Hypertension

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“…The determination of rat urinary kallikrein 1 ), 2 ) has been used äs an Index of activity in the renal kallikrein-kinin System. The activity of this enzyme has been measured by bioassay in the rat isolated Uterus (l, 2), by its esterase activity upon synthetic arginine esters (3) and by its kininogenase activity towards heated plasma or purified fractions from bovine, dog or rat plasma (4,5).…”

Section: Introductionmentioning

confidence: 99%

Specificity of the Amidase and Kininogenase Methods for the Determination of Rat Urinary Kallikrein

Berthoud¹,

Corthorn²

1987

Clinical Chemistry and Laboratory Medicine

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Summary:The specificity of the amidase and kininogenase methods for determining rat urinary kallikrein was studied. Male and female rat urine was employed. Esterase AI, A 2 and kallikrein were separated by DEAE-Sephadex A-50 chromatography. Esterase AI showed no amidase activity towards the Substrate H-£>-Val-Leu-Arg-/?-nitroanilide. In contrast, esterase A 2 and kallikrein attacked the Substrate, and the activity of kallikrein was especially inhibited by aprotinin, while esterase A 2 was more sensitive to soybean trypsin inhibitor. Esterase AI did not show kininogenase activity, whereas esterase A 2 showed this activity, but only towards the dog plasma Substrate. Kallikrein possessed kininogenase activity towards both dog and rat plasma kininogen. We believe that the most specific method for measuring rat urinary kallikrein activity is the kininogenase method using partially purified rat plasma kininogen.

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“…It has also been reported that renal kallikrein might be involved in the pathogenesis of arterial hypertension. Patients with essential hypertension (Margolius et al 1971(Margolius et al , 1974bSeino et al 1975) and experimental animals with hypertension (Croxatto and San Martin 1970;Geller et al 1975;Porcelli et al 1975) excreted less urinary kallikrein than did normotensive controls. Recent papers described the -relationship between kal likrein-kinin system and renin-angiotensin system (Wong et al 1975;Johnston et al 1976) or aldosterone (Margolius et al 1974a).…”

mentioning

confidence: 99%

Effect of furosemide on urinary kallikrein excretion in patients with essential hypertension.

Seino

Abe

Irokawa

et al. 1978

Tohoku J. Exp. Med.

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Kallikrein-like activity in the urine of renal hypertensive rats

Cited by 59 publications

References 0 publications

Immunoreactive glandular kallikrein in plasma during alterations of urinary kallikrein excretion.

Immunoreactive glandular kallikrein in plasma during alterations of urinary kallikrein excretion.

Specificity of the Amidase and Kininogenase Methods for the Determination of Rat Urinary Kallikrein

Effect of furosemide on urinary kallikrein excretion in patients with essential hypertension.

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