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

Seino, Masahide; Abe, Keishi; Irokawa, Nobuo; Ito, Toru; Yasujima, Minoru; Sakurai, Yoshinori; Chiba, Satoru; Saito, Keiichiro; Ritz, Kancho; Kusaka, Takashi; Miyazaki, Seiji; Yoshinaga, Kaoru

doi:10.1620/tjem.124.197

Cited by 12 publications

(2 citation statements)

References 21 publications

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“…1 2 Moreover, patients with essential hypertension and low basal rates of kallikrein excretion have been reported to exhibit blunted increases in PRA associated with concomitantly reduced increments in urinary kallikrein excretion when compared to normal subjects in response to furosemide. 10 In addition, besides our demonstration of its suppressive effect on furosemide-stimulated renin release in the rabbit, 5 aprotinin was subsequently shown to inhibit both of these effects of furosemide simultaneously in the rat. 12 Although components of the kallikrein-kinen system were not measured in our studies, the fact that aprotinin 6 and amiloride 8 both inhibit glandular kallikrein activity strongly suggests that their strikingly similar ability to suppress the stimulated rise in PRA produced by furosemide might be mediated via an inhibition of this system.…”

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confidence: 76%

“…The inhibition of this rise in PRA by amiloride without any significant attenuation of the natriuretic effect of furosemide in the present experiment further strengthens our previous suggestion that the suppression by aprotinin of the furosemide-induced rise in PRA was probably not due to a concomitant suppression of furosemide-induced natriuresis but to an inhibition of renal kallikrein activity. Urinary kallikrein excretion, the commonly used but presumptive index of renal kallikrein activity, is known to be stimulated by furosemide, 10 …”

Section: Discussionmentioning

confidence: 99%

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Inhibition of furosemide-induced increases in plasma renin activity by amiloride.

Shimoda¹,

Lee²,

Maxwell³

1983

Hypertension

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The effect of the potassium-sparing diuretic, amiloride, was studied in conscious rabbits bearing chronic indwelling cannulas to assess whether its reported in vitro kallikrein-inhibiting activity may produce a suppressive effect on furosemide-induced renin secretion similar to that previously demonstrated with another kallikrein inhibitor, aprotinin. Furosemide elicited a rapid and persistent rise in plasma renin activity (PRA), but pretreatment of the same rabbits with a 15-minute intravenous infusion of amiloride, which amounted to 1 mg/kg and commenced at 30 minutes before furosemide, completely prevented this rise. Amiloride also prevented furosemide-induced kaliuresis without an attenuation of the diuretic or natriuretic response and did not alter plasma potassium concentration in the absence of any change in external potassium balance, indicating that suppression of the PRA response is due neither to prevention of extracellular fluid volume contraction nor to the known suppressive effect of hyperkalemia. Mean arterial pressure tended to fall slightly but not significantly with or without amiloride pretreatment. On the basis of these findings and those of our antecedent study with aprotinin, we conclude that the striking similarity between the suppressive effects of two dissimilar inhibitors of kallikrein on pharmacologically evoked renin secretion is consistent with the hypothesis that renal kallikrein participates in the mechanism of renin secretion in vivo. (Hypertension 5: 706-711, 1983) KEY WORDS • renin secretion conscious rabbits kallikrein-kinin system • natriuresis • antikaliuresis U RINARY kallikrein of renal origin 1 has been reported to stimulate renin release in vitro directly by superfused rat renal cortical slices, 2 isolated rat glomeruli, 3 and isolated perfused hog kidneys. 4 In our earler attempt to investigate whether inhibition of kallikrein activity might suppress renin secretion in vivo, 5 we found that both the natriuresis and rise in plasma renin activity (PRA), used as an index of increased active renin secretion, in response to intravenous furosemide administration were markedly attenuated in conscious rabbits by a continuous infusion of aprotinin, a polyvalent bovine proteinase inhibitor that inhibits kallikrein. 6 Since prevention of urinary loss by continuous fluid replacement in our experiment 5 and ureterovenous anastomosis 7 did not prevent the stimu-latory effect of furosemide on PRA, we interpreted our results as indicating that the suppression of the furose-mide-induced rise in PRA by aprotinin was probably not secondary to suppression of natriuresis. However, because aprotinin also inhibits other serine proteases besides kallikrein, 1 6 our observations are only consistent with, but do not prove, the possibilities that renal kallikrein may mediate the release of active renin and participate in the natriuretic action of furosemide. As a logical sequel, we have therefore sought to obtain cor-roborative evidence under similar conditions by using amiloride, an N-amidino pyr...

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confidence: 76%

Section: Discussionmentioning

confidence: 99%

Inhibition of furosemide-induced increases in plasma renin activity by amiloride.

Shimoda¹,

Lee²,

Maxwell³

1983

Hypertension

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Effects of Diuretics on Renal Function

Puschett

Winaver

1992

Comprehensive Physiology

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The sections in this article are: Diuretic Effects on Renal Hemodynamics Drugs That Primarily Alter Glomerular Function Drugs That Primarily Alter Tubular Function Diuretic Effects on Intrarenal Blood Flow Distribution Diuretic Interactions with the Renin–Angiotensin‐Aldosterone system Diuretic Interactions with Prostaglandin Synthesis and with the Inhibition of Prostaglandin Synthetase Nephron Sites of Action and Effects of Diuretics on Solute Excretion Review and Comparison of Methodologies Utility of the Clearance Technique for the Study of Diuretic Site and Mechanism of Action in Man Diuretic Effects on the Excretion of Specific Solutes Cellular and Molecular Actions of Diuretics Carbonic Anhydrase Inhibitors Loop Diuretics Thiazides Mineralcorticoid Antagonists Amiloride

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Renal and Urinary Kallikreins

Ward¹,

Margolius²

1979

Bradykinin, Kallidin and Kallikrein

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

Cited by 12 publications

References 21 publications

Inhibition of furosemide-induced increases in plasma renin activity by amiloride.

Inhibition of furosemide-induced increases in plasma renin activity by amiloride.

Effects of Diuretics on Renal Function

Renal and Urinary Kallikreins

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