A Proposal----The Renal Kallikrein-Kinin System as a Compensating System for Salt Accumulation after Excess Salt Intake

1. The effect of dexamethasone administration for 3 days on urinary kallikrein excretion was studied in 12 normal men with normal sodium intake (n=6) or low sodium intake (n=6). Urinary excretion of sodium, potassium, 17-hydroxycorticosteroids, aldosterone and water was also measured in all subjects. 2. Dexamethasone administration was associated with a significant increase in urinary kallikrein excretion (F3, 30 = 6.9; P < 0.001) regardless of sodium intake. No significant correlation could be established between the increase in urinary kallikrein excretion and changes in urinary sodium, potassium, 17-hydroxycorticosteroids, aldosterone or water. 3. These results suggest that dexamethasone can exert a direct action on the renal kallikrein-kinin system.

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The renal kallikrein-kinin system

AJP Renal Physiology ◽

10.1152/ajprenal.1980.238.4.f247 ◽

1980 ◽

Vol 238 (4) ◽

pp. F247-F255 ◽

Cited By ~ 8

Author(s):

O. A. Carretero ◽

A. G. Scicli

Keyword(s):

Kinin System ◽

Renal Kallikrein ◽

Kallikrein Kinin System

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ALDOSTERONE--A POTENT STIMULATOR OF THE RENAL KALLIKREIN-KININ SYSTEM DURING FETAL LIFE

Pediatric Research ◽

10.1203/00006450-198404001-01651 ◽

1984 ◽

Vol 18 ◽

pp. 368A-368A

Author(s):

Jean E Robillard ◽

Kenneth T Nakamura ◽

Oliva McWeeny ◽

Sindy Wear ◽

William Lawton

Keyword(s):

Fetal Life ◽

Kinin System ◽

Potent Stimulator ◽

Renal Kallikrein ◽

Kallikrein Kinin System

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The Renal Kallikrein-Kinin System: Its Role as a Safety Valve for Excess Sodium Intake, and Its Attenuation as a Possible Etiologic Factor in Salt-Sensitive Hypertension

Critical Reviews in Clinical Laboratory Sciences ◽

10.1080/713609329 ◽

2003 ◽

Vol 40 (1) ◽

pp. 43-115 ◽

Cited By ~ 38

Author(s):

Makoto Katori ◽

Masataka Majima

Keyword(s):

Safety Valve ◽

Sodium Intake ◽

Etiologic Factor ◽

Kinin System ◽

Renal Kallikrein ◽

Excess Sodium ◽

Kallikrein Kinin System ◽

Salt Sensitive Hypertension

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The Renal Kallikrein-Kinin System in Renoparenchymal Hypertension

Advances in Experimental Medicine and Biology - Kinins V ◽

10.1007/978-1-4615-9546-5_21 ◽

1989 ◽

pp. 127-132 ◽

Cited By ~ 1

Author(s):

Toshiaki Ando ◽

Kazuaki Shimamoto ◽

Nobuyuki Ura ◽

Toyoharu Yokoyama ◽

Shuzaburo Fukuyama ◽

...

Keyword(s):

Kinin System ◽

Renal Kallikrein ◽

Kallikrein Kinin System

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Physiological Role of Renal Kallikrein-Kinin System in Human

Advances in Experimental Medicine and Biology - Kinins V ◽

10.1007/978-1-4615-9543-4_13 ◽

1989 ◽

pp. 87-96 ◽

Cited By ~ 3

Author(s):

Kazuaki Shimamoto ◽

Osamu Iimura

Keyword(s):

Physiological Role ◽

Kinin System ◽

Renal Kallikrein ◽

Kallikrein Kinin System

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Bradykinin acutely inhibits activity of the epithelial Na+ channel in mammalian aldosterone-sensitive distal nephron

AJP Renal Physiology ◽

10.1152/ajprenal.00606.2010 ◽

2011 ◽

Vol 300 (5) ◽

pp. F1105-F1115 ◽

Cited By ~ 36

Author(s):

Oleg Zaika ◽

Mykola Mamenko ◽

Roger G. O'Neil ◽

Oleh Pochynyuk

Keyword(s):

Critical Role ◽

Na Channel ◽

Open Probability ◽

Kinin System ◽

Renal Kallikrein ◽

Subsequent Activation ◽

Patch Clamp Electrophysiology ◽

B2 Receptors ◽

Renal Tubular ◽

Kallikrein Kinin System

Activation of the renal kallikrein-kinin system results in natriuresis and diuresis, suggesting its possible role in renal tubular sodium transport regulation. Here, we used patch-clamp electrophysiology to directly assess the effects of bradykinin (BK) on the epithelial Na+ channel (ENaC) activity in freshly isolated split-opened murine aldosterone-sensitive distal nephrons (ASDNs). BK acutely inhibits ENaC activity by reducing channel open probability ( Po) in a dose-dependent and reversible manner. Inhibition of B2 receptors with icatibant (HOE-140) abolished BK actions on ENaC. In contrast, activation of B1 receptors with the selective agonist Lys-des-Arg9-BK failed to reproduce BK actions on ENaC. This is consistent with B2 receptors playing a critical role in mediating BK signaling to ENaC. BK has little effect on ENaC Po when Gq/11 was inhibited with Gp antagonist 2A. Moreover, inhibition of phospholipase C (PLC) with U73122, but not saturation of cellular cAMP levels with the membrane-permeable nonhydrolysable cAMP analog 8-cpt-cAMP, prevents BK actions on ENaC activity. This argues that BK stimulates B2 receptors with subsequent activation of Gq/11-PLC signaling cascade to acutely inhibit ENaC activity. Activation of BK signaling acutely depletes apical PI( 4 , 5 )P2 levels. However, inhibition of Ca2+ pump SERCA of the endoplasmic reticulum with thapsigargin does not prevent BK signaling to ENaC. Furthermore, caffeine, while producing a similar rise in [Ca2+]i as in response to BK stimulation, fails to recapitulate BK actions on ENaC. Therefore, we concluded that BK acutely inhibits ENaC Po in mammalian ASDN via stimulation of B2 receptors and following depletion of PI( 4 , 5 )P2, but not increases in [Ca2+]i.

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Steroid induced changes of the renal kallikrein-kinin system in rats

Acta Endocrinologica ◽

10.1530/acta.0.1070131 ◽

1984 ◽

Vol 107 (1) ◽

pp. 131-140 ◽

Cited By ~ 8

Author(s):

G. Bönner ◽

R. Autenrieth ◽

M. Marin-Grez ◽

G. Speck ◽

F. Gross

Keyword(s):

Urinary Excretion ◽

Time Course ◽

Urine Volume ◽

Renin Angiotensin System ◽

Sprague Dawley ◽

Kinin System ◽

Salt Loading ◽

Renal Kallikrein ◽

Kallikrein Kinin System ◽

Kallikrein Activity

Abstract. In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 × 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 × 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralcorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.

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Influence of sodium balance on urinary excretion of immunoreactive kinins in rats

AJP Renal Physiology ◽

10.1152/ajprenal.1988.254.4.f484 ◽

1988 ◽

Vol 254 (4) ◽

pp. F484-F491 ◽

Cited By ~ 2

Author(s):

J. Barabe ◽

D. Huberdeau ◽

A. Bernoussi

Keyword(s):

Regression Analysis ◽

Urinary Excretion ◽

Sodium Balance ◽

Small Decrease ◽

Sodium Depletion ◽

Urinary Volume ◽

Kinin System ◽

Positive Correlation ◽

Renal Kallikrein ◽

Kallikrein Kinin System

Antibodies against bradykinin (BK) and its metabolites, namely des-Arg9-BK and des-Phe8,Arg9-BK were raised in rabbits, and specific radioimmunoassays (RIA) for these peptides were developed. Specificity studies showed that each RIA was specific for its antigen, since the cross-reactivities of various kinin-related peptides were less than 1.5%. The lowest concentration of peptide that could be measured in these assays was approximately 60 pg/ml. The antibodies were used to measure concentrations of BK and its metabolites in urine and kidneys of rats maintained on different sodium balance for 5 wk. The results showed that normal rats excrete low quantities of BK (63.78 +/- 2.98 ng/day, 88 determinations). The urinary excretion of des-Arg9-BK averaged 77.69 +/- 5.53 ng/day, whereas the amount of des-Phe8,Arg9-BK is equal to 7.13 +/- 0.42 ng/day. Sodium loading brings about a small decrease in the concentration of BK (45.57 +/- 2.36 ng/day, 76 determinations), whereas sodium depletion significantly increased the excretion of BK (94.23 +/- 5.50, 102 determinations, P less than 0.01) accompanied by no modification of the excretion of metabolites. Regression analysis of the results showed a positive correlation between urinary volume and BK in control and sodium-loaded animals and urinary BK and sodium in the sodium-loaded group. In kidney homogenates, sodium depletion increased not only the concentration of BK (10-fold) but also that of des-Arg9-BK and des-Phe8,Arg9-BK by a factor of four and two, respectively, when compared with normal and sodium-loaded animals. These results support the hypothesis that the renal kallikrein-kinin system may be regulated by corticosteroids.

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