Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 184 (1984), S. 171-178 
    ISSN: 1433-8580
    Keywords: Endogenous opioid peptides ; β-Endorphin ; Enkephalins ; Naloxone ; Hemorrhagic hypotension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sixteen anesthetized foxhounds were instrumented for hemodynamic measurements. The adrenolumbar vein was cannulated, and hemorrhagic hypotension (MAP=40 mmHg for 3 h) was induced by bleeding. The plasma levels ofβ-endorphin (β-END), methionine-enkephalin (M-ENK), and leucine-enkephalin (L-ENK) were determined in systemic and adrenal venous blood by specific RIA. Five dogs received an i.v. bolus of naloxone (2 mg/kg) and a subsequent naloxone infusion of 2 mg/kg per hour 1 h after onset of hypovolemia. Eleven dogs served as controls and received equivalent volumes (1 ml/kg per hour) of saline. Hemorrhage resulted in a sharp increase in plasma concentrations of all measured opioid peptides, particularly of M-ENK (26-fold) and L-ENK (24-fold) in the adrenal effluent. Systemicβ-END levels remained 3-fold increased, whereas the ENK release decreased spontaneously. Naloxone treatment inhibited the spontaneous fall of adrenal ENK release during the hypotensive phase; the ENK values remained elevated 20- to 35-fold. Reinfusion of the autologous blood resulted in a normalization of the concentrations of all peptides in both groups. These data demonstrate that hemorrhagic hypotension will cause stimulation of release of endogenous opioid peptides. The high levels of ENK in the adrenal effluent indicate that the adrenal gland is the main source of these peptides in the circulation. In addition toβ-END, the ENK have therefore to be considered as possible factors perpetuating circulatory shock.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 15 (1984), S. 111-118 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In male spontaneously hypertensive rats (SHRSP) of the stroke prone strain (Okamoto) and in normotensive Wistar-Kyoto rats (WKY) urinary kallikrein excretion was investigated at different age and at drug-induced diuresis. In rats of both strains from 7th till 19th week of age urinary kallikrein excretion increased with age. In SHRSP of 7th till 11th week of age kallikrein excretion was higher than in WKY rats, while it was lower in the 48-week-old SHRSP. No correlation was found between urinary kallikrein excretion and systolic blood pressure. In SHRSP and WKY rats a similar daily rhythm of kallikrein excretion in urine was found being high in the early morning and low in the afternoon. Kallikrein excretion correlated significantly with urine volume. The loop diuretic bumetanide (4 and 40 mg/kg) induced diuresis and natriuresis in both strains, however more marked in the WKY rats than in the SHRSP. Urinary kallikrein excretion, however, showed in both strains the same biphasic course with a short lasting increase and a secondary decrease. Thus, in the average urinary kallikrein excretion was not effected by the drug. Prolonged treatment with furosemide over 5 days (125 mg/kg) resulted in an increase in kallikrein excretion in urine, more pronounced in the WKY rats than in the SHRSP. The observed results suggest that renal kallikrein-kinin system is not involved in the development of spontaneous hypertension as a pathogenetic factor, but rather is influenced by other factors like hormone interactions, i.e. mineralocorticoids and catecholamines, as well as renal function and acute changes in urine flow.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 36 (1980), S. 452-454 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The effects of angiotensin II and of the competitive angiotensin II receptor antagonist saralasin on in vivo tumor growth were investigated in hamsters. Angiotensin II strongly inhibited tumor growth while saralasin stimulated it, though the high dose used had partial agonistic angiotensin II-like actions. Lower doses of saralasin were without significant effect on tumor weights.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Intracerebroventricular injections of angiotensin II in anesthetized rhesus monkeys increase systemic blood pressure and heart rate. These effects are accompanied by an increase in plasma ADH, cortisol, adrenaline and noradrenaline. Angiotensin II may participate in central mechanisms of blood pressure regulation by its stimulatory effect on the sympathetic nervous system, on ADH and on ACTH release in primates.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 75 (1982), S. 191-201 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary An antibody against pure rabbit lung converting enzyme (CE) showing cross-reaction with CE from other species was used for immunocytochemical studies in the kidney of rats. Using the indirect labelling PAP-technique, specific immunostaining was found in the endothelial layer of all arteries and arterioles of kidney cortex and in some descending vasa recta. CE-positive reactions were also seen in most glomeruli, the reaction product being confined to only a few capillary loops in connection with the glomerular stalk. A few immunstained capillaries in the cortical labyrinth were suspected to belong to the first ramifications of the efferent arteriole. The bulk of all other of the glomerular and peritubula capillaries as well as all veins of the kidney showed no obvious immunostaining. The functional significance of this specific localization pattern of CE in the endothelium of kidney vessels is discussed with respect to the actions of the systemic and the local, intrarenal reninangiotensin-system on kidney functions.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The distribution of renin and angiotensin II (ANG II) in juxtaglomerular epitheloid cells of control and adrenalectomized rats was studied, using specific antisera and the protein A-gold technique in Lowicryl- and glycol methacrylate-embedded tissue. The matrix of virtually all mature secretory granules of epitheloid cells contains not only renin, but also ANG II. On adrenalectomy, the concentration of both renin and ANG II in the granule internum increases markedly, as indicated by the density of the immunolabel. Given the coexistence of renin and ANG II in the granule matrix, it is quite probable that, with each secretory event, a certain amount of ANG II is released together with renin. Further experiments will have to show if this amount of ANG II cosecreted with renin is sufficient to elicit immediate local intrarenal actions. ANG I, as well as angiotensinogen and converting enzyme, were not found in epitheloid cells. It is therefore inferred that ANG II is not generated intracellularly, but within the extracellular space and subsequently taken up by pinocytosis and incorporated into the secretory granules of epitheloid cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 78 (1983), S. 61-70 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Angiotensin II (ANG II) was localized immunocytochemically in kidney and various other organs of the chinese hamster. In the kidney ANG II-like activity was found in the epitheloid cells of the juxtaglomerular apparatus as well as in the media i.e. the smooth muscle cells of arcuate and interlobular arteries and afferent arterioles. ANG II-like activity was also observed in the medial muscle cells of resistance vessels in other organs and tissues such as submandibular gland and brown adipose tissue. The site of synthesis of ANG II needs to be investigated but the data point to the possibility of an intracellular function of ANG II in smooth muscle cells of blood vessels.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1432-1440
    Keywords: Saralasin ; Angiotensin II ; Renin ; Rezeptoren ; Blutdruck ; Saralasin ; Angiotensin II ; Renin ; Receptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 µg/kg × min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 µg/kg × min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 µg/kg × min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypoor hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.
    Notes: Zusammenfassung Ein verbesserter Test zur Diagnose Renin-abhängiger Bluthochdruckformen mit dem Angiotensin II Rezeptor Antagonisten Saralasin wurde in hypertensiven Ratten, sowie in normotensiven und hypertensiven Patienten geprüft. Kumulative intravenöse Dosen, beginnend mit 0,01 µg/kg × min Saralasin wurde alle 15 Minuten um das zehnfache gesteigert. Ein signifikanter Blutdruckabfall bei der Dosis von 0,1 µg/kg × min wurde bei Ratten mit renaler Hypertonie, bei Patienten mit renaler Hypertonie und bei Patienten nach Diuretika-Vorbehandlung gefunden. Plasmaspiegel von Angiotensin I, Angiotensin II, Plasma Renin Aktivität und Saralasin wurden gemessen. Bei der niedrigsten Infusionsrate von 0,01 µg/kg × min waren die Saralasin-Konzentrationen im Plasma 40fach höher als die Plasma Angiotensin II-Konzentrationen. Der Blutdruckabfall erfolgte bei niedrigeren Dosen von Saralasin als der Anstieg von Plasma-Renin als Folge einer Hemmung des feedbacks der Reninsekretion. Die Ergebnisse zeigen, daß Komplikationen wie schwerwiegende Blutdruckanstiege und -abfälle bei schrittweiser Erhöhung der Saralasin-Infusionsrate vermieden werden können; gleichzeitig wird die diagnostische Zuverlässigkeit des Tests erhöht. Der geringe Angiotensin-ähnliche, blutdrucksteigernde Effekt von Saralasin bei Patienten mit niedrigem Renin wird als Vorteil ausgenutzt und erhöht den Unterschied der Blutdruckantwort bei Patienten mit hohem Plasma-Renin und Blutdruckabfall nach Saralasin-Infusion.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...