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  • 1
    ISSN: 1432-1440
    Keywords: ANP ; Renal failure ; Hemodynamics ; Renal function ; Sodium homeostasis ; Renin-aldosterone-axis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the effects of 60 minα-hANP infusion (24 ng/min/kg) on glomerular filtration rate (GFR), renal blood flow (RBF), cardiac index (CI) and blood pressure (BP) in 8 patients with chronic renal failure (CRF) with GFR ranging from 18 to 80 ml/min/1.73 m2 and in 8 control (C) subjects with normal renal function. Basal plasma levels of ANP and cGMP were elevated in CRF (ANP: 60.6±9.1 vs 13.6±1.9 pmol/l,p〈0.05; cGMP: 14.3±2.9 vs 6.6±1.1 pmol/ml,p〈0.05). During ANP infusion, peak levels of cGMP were higher in CRF than in C (27.5±3.2 vs. 17.3±1.3 pmol/ml,p〈0.05). During ANP infusion, GFR increased in CRF by 70.7±4.2% from 34.5±6.8 to 57.4±9.9 ml/min/1.73m2 (p〈0.001) as compared to 16.2±1.4% in C (p〈0.001 vs CRF). RBF increased in CRF by 43.6±6.4% and in C by 3.1±1.2% (p〈0.01). Basal urinary sodium excretion (UNaV) was slightly lower in CRF than in C but rose to the same level in both groups during ANP infusion. In CRF, as opposed to C, UNaV remained elevated above baseline after the end of the infusion. The effect of ANP on fractional sodium excretion (FENa), however, was more pronounced in C. Basal FENa was higher in CRF (12.8±2.5% vs 2.4±1.5% in C,p〈0.001), FENa remained elevated at 180% over baseline in C sixty minutes after cessation of ANP infusion, while it had returned to baseline in CRF. During ANP infusion, CI increased in CRF after 30 min from 2.91±0.08 to 3.12±0.091/min/m2 (p〈0.001) and in C from 3.20±0.11 to 3.39±0.13 l/min/m2 (p〈 0.05). Mean arterial BP was higher in CRF and its decrease was greater than in C (21.1±2.7% vs 9.1±1.0%,p〈0.001). In patients with CRF GFR, RPF, and CI remained significantly elevated and BP was still significantly decreased 60 min after ANP infusion. Total peripheral vascular resistance (TPR) was elevated in CRF and declined during ANP infusion in both CRF and C. The decline of TPR was sustained and more pronounced in CRF than in C. Renal vascular resistance (RVR) was high in CRF and dropped by nearly 50% during ANP infusion, whereas only a moderate decline in RVR during ANP application was observed in C. Thus, exogenous ANP had greater and prolonged effects on systemic hemodynamics and renal function in CRF than in C. They may be due to higher levels of ANP following ANP infusion and appear to be mediated by a more sustained formation of the second messenger cGMP.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 1234-1239 
    ISSN: 1432-1440
    Keywords: 8-arginine-vasopressin ; Hemodynamic effects ; inhibition of prostaglandin synthesis ; Renin ; Hypertension ; 8-Arginin-Vasopressin ; Hämodynamische Wirkungen ; Hemmung der Prostaglandin-Synthese ; Renin ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bisher vorliegende Untersuchungen lassen vermuten, daß in einem normotensiven Organismus der vasopressorische Effekt von 8-Arginin-Vasopressin (AVP) effektiv durch cardiovaskuläre Reflexe abgeschwächt wird. Die Gabe von exogenem AVP führt zu nur vorübergehenden Pressorreaktionen trotz fortgeführter ADH-Infusion und deutlich erhöhter Plasma-AVP-Konzentrationen. Die vorliegende Untersuchung versucht den Mechanismus der nur vorübergehenden Blutdruckerhöhungen, die oft als “Tachyphylaxie” bezeichnet werden, weiter zu charakterisieren. Unsere Ergebnisse bei gesunden Versuchspersonen zeigen einen zweiphasigen Verlauf nach i.v. Gabe von AVP: eine initiale Phase, die durch cardiovaskuläre Reflexe gekennzeichnet ist und eine zweite Phase, während der sich der periphere Gefäßwiderstand normalisiert. Hemmung der Prostaglandin-Synthese mit Indomethacin schwächt die vaskuläre Gegenregulation auf exogenes AVP ab und läßt so eine prostaglandinvermittelte Vasodilatation als Reaktion auf AVP als Ursache der „Vasopressintachyphylaxie“ vermuten. Die Bedeutung des Renin-Angiotensin-Systems und unterschiedlicher regionaler hämodynamischer Effekte von AVP werden diskutiert.
    Notes: Summary Previous investigations suggest that in a normotensive organism the vasopressor effect of 8-arginine-vasopressin (AVP) is very effectively buffered by cardiovascular reflex mechanisms. Exogenous AVP administration shows only small, transient increases in blood pressure in spite of continued AVP-infusion and high plasma AVP concentrations. The present study aims to clarify the mechanism of the observed transient blood pressure elevations which are often referred to as “tachyphylaxis”. Our results in healthy subjects show a two phase response to exogenous AVP: an initial phase which is characterized by cardiac reflex mechanisms and a second phase during which a normalisation of the elevated total peripheral resistance occurs. Inhibition of prostaglandin synthesis with indomethacin almost completely attenuates this vascular counterregulation to exogenous AVP, thus providing evidence that a prostaglandin mediated vasodilation in response to AVP may be the underlying mechanism for “vasopressin tachyphylaxis”. The role of the renin-angiotensin-system and the importance of different regional hemodynamic effects of AVP are discussed.
    Type of Medium: Electronic Resource
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