Urinary Kallikrein Excretion in Bartter's Syndrome

Lechi, Alessandro; Covi, G; Lechi, C.; Mantero, Franco; Scuro, L.A.

doi:10.1210/jcem-43-5-1175

Cited by 47 publications

(19 citation statements)

References 13 publications

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“…Consistent with this observation are the report by Lechi et al (45) and otir presenit findings that patients with Bartter's syndrome excrete more kallikreini than normiial subjects. Indeed, patients with Bartter's syndrome excreted three times as mutchi kallikrein as soditum-replete normal subjects, but only one-third more than sodiulm-depleted normal subjects.…”

Section: Discussionsupporting

confidence: 78%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

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A B S T R A C T The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+5.3 (S.E.M.) ng/ml per h to 3.3±1.1 ng/ml per h, mean plasma bradykinini (patients recumbent) from 15.4±4.4 ng/ml to 3.9±0.9 ng/ml, mean urinary kallikrein excretion from 24.8±3.2 tosyl-arginine-methyl ester units (TU)/ day to 12.4±2.0 TU/day, but increased mean urinary kinin excretion from 3.8±1.3 ,ug/day to 8.5±2.5 ,ug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for uriniary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The

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Section: Discussionsupporting

confidence: 78%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

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“…In fact, a large accumulation of data indicates a positive correlation between the activity of sodium-retaining steroid hormone and the renal kallikrein-kinin system. Urinary excretion of kallikrein is increased 1) in patients with primary aldosteronism (48), 2) in normal volunteers or patients with essential hypertension on a diet of low sodium or high potassium (121), 3) after treatment with 9α-fluorohydrocortisone (126), and 4) in Bartter's syndrome (hypertrophy and hyperplasia of the juxtaglomerular cells, producing hypokalemic alkalosis and hyperaldosteronism) (127). In addition, treatment of patients affected by primary aldosteronism and treatment of normal volunteers with spironolactone, a selective antagonist of aldosterone, markedly reduced urinary kallikrein excretion (121,128).…”

Section: ) Sodium-retaining Steroid Hormonesmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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Abstract. It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (K ATP ) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as K ATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.

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“…In humans and rats, sodium-retaining steroids or maneuvers which increase aldosterone activity, such as reduced dietary sodium or increased dietary potassium increase renal and urinary kallikrein activity; whereas spironolactone reduces it (3)(4)(5)(6)(7)(8)(9). Kallikrein excretion is elevated in primary aldosteronism or Bartter's syndrome (10)(11)(12)(13). In the rat kidney, kallikrein is localized at the apical portions of cells of the distal nephron (14,15) and is membrane bound (16).…”

Section: Introductionmentioning

confidence: 99%

Amiloride inhibits mammalian renal kallikrein and a kallikrein-like enzyme from toad bladder and skin.

Margolius¹,

Chao²

1980

J. Clin. Invest.

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A B S T R A C T Renal kallikrein is localized in luminal plasma membranes of the mammalian distal nephron and gains access to urine from this site. Its activity is regulated, in part, by aldosterone. These facts led us to study the effects of amiloride, a drug known to inhibit sodium reabsorption and potassium secretion at this site, on kallikrein activity. Amiloride inhibited the esterolytic activity of purified rat or human urinary kallikrein or of rat renal cortical cells upon a synthetic substrate (ID50 = 0.12-0.23 mM). Kinetic analyses showed that the enzyme inhibition was noncompetitive and reversible in nature. The kinin-generating activity of kallikrein acting upon kininogen substrates was also inhibited by amiloride, as measured by bioassay in the rat uterus or guinea pig ileum or by radioimmunoassay of liberated kinins (ID50 = 85 A.tM). No other diuretic drug tested inhibited kallikrein activity, except triamterene, which did so, weakly. In addition, kallikrein-like enzyme activity was discovered in the urinary bladder or skin of Bufo marinus toads and this activity was also inhibited by amiloride. The localization ofthe enzyme and its inhibition by this drug suggest that further study of relationships amongst the glandular kallikrein-kinin system and renal ion and water transport is warranted.

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Urinary Kallikrein Excretion in Bartter's Syndrome

Cited by 47 publications

References 13 publications

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Amiloride inhibits mammalian renal kallikrein and a kallikrein-like enzyme from toad bladder and skin.

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