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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 42 (1986), S. 1238-1239 
    ISSN: 1420-9071
    Keywords: Kinins ; bradykinin ; kallidin ; cerebrospinal fluid ; HPLC ; hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Rat cerebrospinal fluid contains peptides which displace radiolabeled bradykinin from its specific antibodies. Two peptides which showed the same retention time as kallidin and bradykinin in a reverse phase high pressure liquid chromatography system were detected in cerebrospinal fluid of rats. The concentration of radioimmunologically detected kinins in the cerebrospinal fluid of spontaneously hypertensive rats of the Okamoto strain was lower than that of the Wistar Kyoto control rats.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Immunocytochemistry ; Juxtaglomerular apparatus ; Renin ; Angiotensin ; Angiotensinogen ; Converting enzyme ; Immunzytochemie ; Juxtaglomerulärer Apparat ; Renin ; Angiotensin ; Angiotensinogen ; Converting enzyme
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die intrarenale Verteilung von Renin, Converting enzyme (CE) und Angiotensin II (ANG II) wurde mit immunzytochemischen Methoden an Ratten und Mäusen untersucht. Die hier aufgezeigten spezifischen Verteilungsmuster dieser Komponenten des Renin-Angiotensin-Systems (RAS) legen die Annahme nahe, daß es neben den bekannten systemischen, durch ANG II vermittelten Effekten des RAS auch lokale Interaktionen von RAS-Bestandteilen innerhalb der Niere gibt. — Eine erste Folge dieser Interaktionen dürfte die intrarenale Generation einer zusätzlichen Portion von ANG II im Nierenblutstrom sein, deren Zielgebiet durch die spezifische Lokalisation von CE in bestimmten Endothelbereichen der Nierenstrombahn bestimmt wird. Solche intrarenal-intravasalen Reaktionen können für sich wirksam werden, aber auch den Effekt von „systemisch“, d.h. prärenal generiertem ANG II verstärken. — Unsere Ergebnisse sprechen weiter dafür, daß es neben diesen intrarenal-intravasalen auch echte intrarenal-interstitielle Interaktionen der RAS-Komponenten gibt, deren Wirkung sich über das im Interstitium der Nierenrinde generierte ANG II allein auf die Niere beschränkt. Für das Vorhandensein eines solchen lokal-intrarenalen RAS spricht vor allem der Nachweis von ANG II in den epitheloiden Zellen des JGA und die Dissoziation des systemischen — an der Plasmakonzentration abzulesenden — Renin und ANG II von deren lokal-intrarenalen Konzentrationen bei renal hypertensiven Ratten.
    Notes: Summary The localization of renin, converting enzyme (CE) and angiotensin II (ANG II) in the kidneys of rats and mice was investigated with immunocytochemical methods. According to the presence and specific intrarenal localization of these components of the renin-angiotensin-system (RAS) our results suggest that in addition to the well known systemic effects of the RAS, there are interactions of its components inside the kidney. These interactions may lead to the generation of an extra portion of ANG II in the renal blood stream with its target cells determined by the localization of CE at the luminal side of well defined endothelial areas. These intrarenal-intravasal reactions may or may not reinforce the action of “systemic” ANG II, generated prerenally. In addition, the existence of true intrarenal-interstitial interactions, with the different components and actions of this intrarenal RAS restricted entirely to the kidney is suggested by our results, particularly the demonstration of ANG II within epitheloid cells and the dissociation of systemic renin and ANG II from their local concentrations in renal hypertensive rats.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 36 (1980), S. 865-866 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Rat urine, even at a 1∶10 final dilution in Tyrode's solution, stimulates contraction of the ureteral musculature in vitro. This effect can be ascribed to the presence of kallikrein or a kallikrein-like enzyme in urine. Isometric contractions of ureters were prevented by previous addition of aprotinin to the organ bath. Urine also lost its activity after inactivation of enzymes by heat or acid treatment.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 38 (1982), S. 941-943 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Adrenalectomy reduces, and sodium depletion increases, both the daily urinary excretion of kallikrein and the kallikrein activity in the renal cortex. These 2 variables were found to correlate significantly in normal, sodium depleted and adrenalectomized rats, thus supporting the view that kallikrein excretion reflects the activity of the enzyme in the kidney.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 324 (1986), S. 473-476 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The lack of effect of ANP on sodium transport in vitro suggests that reduction of sodium reabsorption in vivo may be secondary to another process, perhaps to renal vasodilatation. Renal vasodilators cause natriuresis5. ANP both lowers the vascular resistance of the pre-constricted isolated perfused ...
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The immunoreactivity for renin and angiotensin II (ANG II) in the ischaemic and non-ischaemic kidney of rats with renovascular hypertension was compared with that of the kidneys of sham operated controls. In addition, the renin concentration of these kidneys and the plasma level of ANG II were determined in hypertensive and control animals. In parallel with the renin concentration of kidney cortex, the immunoreactivity, i.e. the JG-index for renin of the afferent arterioles from the ischaemic kidney was slighly increased, that from the nonischaemic kidney drastically decreased as compared to control kidneys. Similarly, the JG-index for ANG II was increased in the ischaemic and decreased in the non-ischaemic kidney although the plasma level of ANG II was elevated in the animals with renovascular hypertension. This difference in the immunocytochemically detectable ANG II and especially the decrease of ANG II in the non-ischaemic kidney in spite of elevated plasma ANG II levels is interpreted to result from similar differences in the local (extravascular) formation of ANG II by the intrarenal renin-angiotensin system.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2013
    Keywords: Key words Kallikrein ; Acid-base balance ; Acidosis ; Renal function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of altering the acid-base status on urinary kallikrein excretion of barbiturate-anaesthetized rats was investigated. Alkalosis was induced in a group of rats by intravenous (i.v.) infusion of NaOH at 0.45 mmol ⋅h−1 for 30 min. Acidosis was induced in two groups of rats by i.v. infusion of HCl at 1.5 mmol⋅h−1 for 30 min (uncompensated acidosis) or 0.15 mmol⋅h−1 for 3 h (compensated acidosis), respectively. Time controls received 0.45 mmol⋅h−1 NaCl. Rats with alkalosis excreted less kallikrein than their controls (P 〈 0.05). Rats with uncompensated acidosis excreted more active kallikrein (P 〈 0.05), whereas rats with compensated acidosis excreted similar amounts when compared with their respective controls. In rats with uncompensated acid-base derangements, the urinary kallikrein excreted per millilitre of glomerular filtrate was correlated with blood H+ activity (r = 0.99, P 〈 0.01). Arterial blood pressure, haematocrit, glomerular filtration rate, urine flow rate and Na+ and K+ excretions of experimental and control animals did not differ. Thus, renal kallikrein secretion into the tubular fluid appears to be regulated by blood proton activity. This, along with our previous demonstration that kallikrein inhibits HCO3 − secretion into the tubular lumen (Renal Physiol 17:301–306, 1994; J Physiol (Lond) 488:163–170, 1995), indicates that this enzyme is part of a feedback loop regulating acid-base balance.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 39 (1983), S. 360-362 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Purified urinary kallikrein induces contractions of the rat ureter in vitro. Antibodies against kallikrein block the contractile response of the isolated ureter to rat urine.
    Type of Medium: Electronic Resource
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