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  • Angiotensinogen  (3)
  • Propranolol  (2)
  • [abr] ANP; atrial natriuretic peptide  (2)
  • Angiotensin I-converting enzyme  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 139 (1986), S. 266-274 
    ISSN: 0006-291X
    Keywords: [abr] ANP; atrial natriuretic peptide ; [abr] Bbr-cGMP; 8-bromo-cyclicGMP ; [abr] SNP; sodium nitroprusside ; [abr] TPA; 12-0-tetradecanoyl-phorbol-13-acetate ; [abr] db-cAMP; dibuturyl-cyclicAMP
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 139 (1986), S. 266-274 
    ISSN: 0006-291X
    Keywords: [abr] ANP; atrial natriuretic peptide ; [abr] Bbr-cGMP; 8-bromo-cyclicGMP ; [abr] SNP; sodium nitroprusside ; [abr] TPA; 12-0-tetradecanoyl-phorbol-13-acetate ; [abr] db-cAMP; dibuturyl-cyclicAMP
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Angiotensin I-converting enzyme ; Gene expression ; Sodium chloride ; Heart ; Inbred rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have recently shown that the angiotensin I converting enzyme (ACE) gene is linked to NaCl-loaded blood pressure in the stroke-prone spontaneously hypertensive rat (SHRSP), and that high-NaCl loading selectively stimulates ACE in the aorta of SHRSP but not in normotensive Wistar-Kyoto (WKY) rats. We therefore investigated the relationship between cardiac ACE and the development of hypertension and left ventricular hypertrophy in response to normal- and high-NaCl diet in these rats. ACE mRNA and ACE activity were measured in left ventricular tissue after completion of hemodynamic characterization of the animals. While SHRSP rats increased blood pressure (P〈0.0001) and heart rate (P〈0.005) in response to high NaCl, blood pressure remained unchanged in WKY. Similarly, relative left ventricular weight increased only in SHRSP after high NaCl (P〈0.002). A significant two- to threefold increase of cardiac ACE mRNA and fourfold stimulation of ACE enzyme activity in response to high NaCl was found in both WKY and SHRSP rats (P〈0.005). The induction of ACE gene expression was significantly more pronounced in SHRSP compared to WKY (P〈0.02), whereas no significant strain differences in left ventricular ACE activity were found after either normal- or high-NaCl diet. Thus, arterial blood pressure and left ventricular weight remained unchanged in the WKY rats despite the activation of left ventricular ACE activity after high-NaCl exposure. These results demonstrate that left ventricular ACE activity is equally upregulated in response to high-NaCl in the normotensive and hypertensive strain, independently from the development of hypertension. We conclude that the pretranslational induction of left ventricular ACE with high-NaCl loading may be important both for the regulation of cardiac angiotensins and kinins and for local therapeutic ACE inhibition in the heart during high-salt status.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Regulatory Peptides 46 (1993), S. 487-509 
    ISSN: 0167-0115
    Keywords: Angiotensin II ; Angiotensin II receptor ; Angiotensin-converting enzyme ; Angiotensinogen ; Renin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    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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  • 6
    ISSN: 1432-1440
    Keywords: Blutdruck ; Angiotensin II ; Propranolol ; Spontan hypertensive Ratten ; Gehirn ; Blood pressure ; Angiotensin II ; Propranolol ; Spontaneously hypertensive rats ; Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The blood pressure responses following infusions of angiotensin II (ANG II) into the brain ventricles (i.v.t.) have been tested in spontaneously hypertensive (SH) rats and in normotensive Wistar Kyoto (WK) rats. The mean arterial blood pressure increases were significantly higher in SH rats than in WK rats. Propranolol treatment reduced blood pressure increases to i.v.t. ANG II in WK, but not in SH rats. The higher sensitivity to i.v.t. ANG II in SH rats supports a role of central ANG II in the maintenance of high blood pressure in SH rats.
    Notes: Zusammenfassung Angiotensin II (ANG II) wurde spontan hypertensiven (SH) Ratten und normotensiven Wistar Kyoto (WK) Ratten in den lateralen Hirnventrikel (i.v.t.) infundiert. Der mittlere arterielle Blutdruck stieg bei den SH Ratten signifikant höher an als bei den normotensiven WK Ratten. Propranolol-Vorbehandlung reduzierte die Blutdruckanstiege nach i.v.t. ANG II Infusionen bei WK Ratten, nicht aber bei SH Ratten. Die höhere ANG II Empfindlichkeit der SH Raten bestätigt frühere Ergebnisse, die darauf hinweisen, daß zentrales ANG III an der Aufrechterhaltung des hohen Blutdruckes von SH Ratten beteiligt sein kann.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 43-45 
    ISSN: 1432-1440
    Keywords: Gehirnrenin ; Angiotensin ; Angiotensinogen ; Liquor cerebrospinalis ; Blutdruck ; Brain renin ; Angiotensin ; Angiotensinogen ; Cerebrospinal fluid ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Cerebrospinal fluid (CSF) of rats contains high angiotensinogen concentrations. When 3500-fold purified renin from human brain was injected into the brain ventricles of rats, angiotensin I concentrations increased from undetectable levels to 147.9±18.8 fMol per ml CSF. In parallel, mean arterial blood pressure increased from 93±2.4 mm Hg to 107±3.7 mm Hg. The increase in blood pressure could be abolished by intraventricular administration of saralasin, a blocker of angiotensin II receptors. Intraventricular injection of cathepsin D had no effect on arterial blood pressure and the angiotensin I concentration in CSF remained below detection limits of the radioimmunoassay. We conclude that brain renin acts on endogenous brain angiotensinogen under physiological in vivo conditions to form angiotensin I. The latter is converted to angiotensin II and leads to biological effects, i.e. increase of blood pressure.
    Notes: Zusammenfassung Der Liquor cerebrospinalis von Ratten enthält Angiotensinogen in hoher Konzentration. Nach Injektion von 3500fach angereichertem menschlichem Gehirnrenin in die Hirnventrikel von Ratten stieg die Konzentration von Angiotensin I von unmeßbar niedrigen Werten auf 147,9±18,8 fMol pro ml Liquor an. Der mittlere arterielle Blutdruck änderte sich dabei von 93±2,4 mm Hg auf 107±3,7 mmHg. Der Blutdruckanstieg konnte durch intraventrikuläre Gabe des Angiotensin II Rezeptorenblockers Saralasin rückgängig gemacht werden. Die intraventrikuläre Injektion von Cathepsin D hatte keinen Effekt auf den arteriellen Blutdruck, und die Angiotensin I Konzentration im Liquor blieb unterhalb des Meßbereiches des Radioimmunoassays. Wir schließen daraus, daß Gehirnrenin unter physiologischen Bedingungen in vivo Angiotensin I von endogenem Gehirnangiotensinogen abspaltet. Angiotensin I wird zu Angiotensin II umgewandelt und führt zum Blutdruckanstieg.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 15-20 
    ISSN: 1432-1912
    Keywords: Diazoxide ; Propranolol ; Tachycardia ; Hypotension ; Hyperglycaemia ; Sympathetic reflex activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In unanaesthetized rabbits, diazoxide was injected i.v. in doses of 6.25, 12.5, and 25.0 mg/kg. A dose-dependent fall in blood pressure occurred, while heart rate rose to nearly maximum levels already with the lowest dose. After the medium and the high dose, blood glucose concentration increased continuously within the observation period of 2 h, and plasma concentration of angiotensin II was about 10-fold normal after the same time. Propranolol in doses of 0.67, 2.0, and 6.0 mg/kg, given i.v. 15 min before diazoxide (12.5 mg/kg), had no effect on the hypotensive action of the latter, but inhibited the increase both in heart rate and in blood pressure. The initial rise in heart rate was partly inhibited by 2 mg/kg propranolol, but no further inhibition was obtained by the dose of 6 mg/kg. Blood glucose increase was abolished by 2 mg/kg and markedly suppressed by 6 mg/kg propranolol. Beta-adrenoceptor blockade also reduced the elevated plasma concentration of angiotensin II. It is concluded that the rise in heart rate induced by diazoxide is caused not only by sympathetic stimulation, but also by a direct action on the heart. Similarly, the increase in plasma angiotensin II concentration is in part induced by beta-adrenoceptor stimulation and in addition by a direct renal mechanism. On the other hand, the hyperglycaemic effect seems to depend predominantly upon the stimulation of beta-adrenoceptors.
    Type of Medium: Electronic Resource
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