Stimulation of the Renal Kallikrein-Kinin System by Vasoactive Substances and Its Relationship to the Excretion of Salt and Water1

2015 ◽  
pp. 132-144 ◽  
Author(s):  
Ivor H. Mills ◽  
L. F. O. Obika ◽  
Pamela A. Newport
Keyword(s):  
Kinin System ◽  
Vasoactive Substances ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Stimulation Of

The renal kallikrein-kinin system

1980 ◽  
Vol 238 (4) ◽  
pp. F247-F255 ◽  
Author(s):  
O. A. Carretero ◽  
A. G. Scicli
Keyword(s):  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

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

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

The Renal Kallikrein-Kinin System in Renoparenchymal Hypertension

1989 ◽  
pp. 127-132 ◽  
Author(s):  
Toshiaki Ando ◽  
Kazuaki Shimamoto ◽  
Nobuyuki Ura ◽  
Toyoharu Yokoyama ◽  
Shuzaburo Fukuyama ◽  
...  
Keyword(s):  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

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

2011 ◽  
Vol 300 (5) ◽  
pp. F1105-F1115 ◽  
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.

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

1984 ◽  
Vol 107 (1) ◽  
pp. 131-140 ◽  
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.

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

1988 ◽  
Vol 254 (4) ◽  
pp. F484-F491 ◽  
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.

scholarly journals Antihypertensive effect of MK-421 in rats. Role of the renal kallikrein-kinin system.

Hypertension ◽  
1984 ◽  
Vol 6 (2_pt_1) ◽  
pp. 229-235 ◽  
Author(s):  
M Yasujima ◽  
K Abe ◽  
M Tanno ◽  
Y Kasai ◽  
J Tajima ◽  
...  
Keyword(s):  
Antihypertensive Effect ◽  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

Potassium supplement upregulates the expression of renal kallikrein and bradykinin B2receptor in SHR

1999 ◽  
Vol 276 (3) ◽  
pp. F476-F484 ◽  
Author(s):  
Lan Jin ◽  
Lee Chao ◽  
Julie Chao
Keyword(s):  
Blood Pressure ◽  
Tissue Kallikrein ◽  
Mrna Levels ◽  
High Potassium ◽  
Kinin System ◽  
Glomerular Lesion ◽  
Potassium Supplement ◽  
Potassium Intake ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

High potassium intake is known to attenuate hypertension, glomerular lesion, ischemic damage, and stroke-associated death. Our recent studies showed that expression of recombinant kallikrein by somatic gene delivery reduced high blood pressure, cardiac hypertrophy, and renal injury in hypertensive animal models. The aim of this study is to explore the potential role of the tissue kallikrein-kinin system in blood pressure reduction and renal protection in spontaneously hypertensive rats (SHR) on a high-potassium diet. Young SHR were given drinking water with or without 1% potassium chloride for 6 wk. Systolic blood pressure was significantly reduced beginning at 1 wk, and the effect lasted for 6 wk in the potassium-supplemented group compared with that in the control group. Potassium supplement induced 70 and 40% increases in urinary kallikrein levels and renal bradykinin B2 receptor density, respectively ( P < 0.05), but did not change serum kininogen levels. Similarly, Northern blot analysis showed that renal kallikrein mRNA levels increased 2.7-fold, whereas hepatic kininogen mRNA levels remained unchanged in rats with high potassium intake. No difference was observed in β-actin mRNA levels in the kidney or liver of either group. Competitive RT-PCR showed a 1.7-fold increase in renal bradykinin B2 receptor mRNA levels in rats with high potassium intake. Potassium supplement significantly increased water intake, urine excretion, urinary kinin, cAMP, and cGMP levels. This study suggests that upregulation of the tissue kallikrein-kinin system may be attributed, in part, to blood pressure-lowering and diuretic effects of high potassium intake.

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