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  • 1
    Electronic Resource
    Electronic Resource
    Erniedrigte renale Prostaglandin E2-Ausscheidung und verminderte Stimulierbarkeit der Plasmareninaktivität bei Patienten mit essentieller Hypertonie (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 567-573 
    Details
    ISSN: 1432-1440
    Keywords: Renal prostaglandins ; Essential hypertension ; Plasma renin activity ; Renale Prostaglandine ; essentielle Hypertonie ; Plasmareninaktivität
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die renale Prostaglandin (PG)-Ausscheidung und die Stimulierbarkeit der Reninsekretion wurde bei Patienten mit essentieller Hypertonie (n=35) und bei altersgleichen normotensiven Kontrollpersonen (n=22) vergleichend untersucht. Bei den Patienten mit essentieller Hypertonie wurde eine erniedrigte basale Ausscheidung des vasodilatierenden PGE2 (p〈0,02) bei im Normbereich liegender Ausscheidung des vasokonstriktorischen PGF2α im Urin festgestellt. Darüber hinaus stieg innerhalb der ersten 15 min nach i.v.-Gabe von 40 mg Furosemid die PGE2-Ausscheidung bei Patienten mit essentieller Hypertonie signifikant geringer an als bei den Kontrollpersonen (p〈0,001), während der Anstieg der PGF2α-Ausscheidung in beiden Gruppen gleich war. Zum gleichen Zeitpunkt lag der prozentuale Anstieg der Plasmareninaktivität nach Furosemid bei Hypertonikern (167±11 (SEM)) deutlich unter dem Anstieg der Kontrollgruppe (386±46,p〈0,001). Unsere Ergebnisse unterstützen die Annahme, daß eine erniedrigte renal-kortikale, (vaskuläre?) Synthese vasodilatierender Prostaglandine die Ursache sowohl für die verminderte Stimulierbarkeit der Reninsekretion als auch für den gesteigerten renalen Gefäßwiderstand bei essentieller Hypertonie ist.
    Notes: Summary Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age-and sex-matched controls (p〈0.02). PGF2α-excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p〈0.001), while the increase in PGF2α-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167%±11, SEM) than in the normotensive (386%±46) group (p〈0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01491135
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  • 2
    Electronic Resource
    Electronic Resource
    Renal prostaglandins: Relationship to the development of blood pressure and concentrating capacity in pre-term and full term healthy infants (1979)
    Springer
    European journal of pediatrics 132 (1979), S. 253-259 
    Details
    ISSN: 1432-1076
    Keywords: Renal prostaglandins ; cAMP ; Blood pressure ; Concentrating capacity ; Neonatal period
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationships between urinary prostaglandins (PGs)E2 and F2α and the postnatal development of blood pressure and renal concentrating capacity were investigated in 14 pre-term and 32 full term healthy infants. Mean PGE2 and PGF2α excretion was 18.9 and 10.1 ng/h/1.73 m2, respectively, in pre-term infants. In full term infants mean urinary PGE2 was signifincantly lower (13.4 ng/h/1.73 m2) and PGF2α significantly higher (22.2 ng/h/1.73 m2). The decrease of the PGE2/PGF2α ratio (P〈0.001) was accompanied by an increase in blood pressure. High PGE2 levels in pre-term infants were inversely correlated with urinary cAMP excretion. A decreasing PGE2/PGF2α ratio in full term infants was associated with increasing urinary osmolality. After intranasal administration of antidiuretic hormone (DDAVP) in 8 full term infants the increase in urinary osmolality and cAMP excretion was accompanied by a drop in PGE2 excretion to less than half the basal values. These findings suggests that the postnatal changes in urinary PG excretion are associated with a concomittant increase in blood pressure and in the concentrating capacity of the neonatal kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00496848
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of inhibition of prostaglandin synthesis on tubuloglomerular feedback in the rat kidney (1979)
    Springer
    Pflügers Archiv 379 (1979), S. 269-279 
    Details
    ISSN: 1432-2013
    Keywords: Micropuncture ; Rat kidney ; Tubuloglomerular feedback ; Prostaglandin inhibitors ; Renal prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To further clarify the mechanism mediating the reduction of nephron filtration rate in response to an increase of loop of Henle flow rate we have studied the effect of prostaglandin inhibition on tubuloglomerular feedback in rats. Following inravenous administration of 2 or 5 mg/kg indomethacin feedback responses expressed as the percent reduction of early proximal flow rate (EPFR) during flow elevation from 0–40 nl/min decreased from control values of −54.3±4.3% (mean ± S.E.) and −39.5±3.9% to −27.9±2.8% (P〈0.001) and −5.0±4.9% (P〈0.001) respectively. A significant reduction in the feedback response was also seen following intravenous administration of 2 or 5 mg/kg Ro 20-5720 (−28.8±5.8% and −7.8±3.8% respectively), 10 mg/kg meclofenamate (−15±4%), and 2 mg/kg eicosa-5,8,11,14-tetraynoic acid (−16.2±4.8%). In contrast to control animals injection of 5 mg/kg indomethacin had no effect on the feedback response in rats kept on a low salt diet. After applying a single dose of 5 mg/kg indomethacin or Ro 20-5720 feedback responses were reduced to −5.4±4.3% and −3.0±4.36% in the period 0–80 min, but were normal in the period 81–160 min after injection (−36.1±2.83% and −44.3±2.82% respectively). A dose dependent inhibition of the feedback response was also noted when indomethacin was applied intraluminally with full inhibition being established at a concentration of 0.5 mM. Urinary excretion rates of PGE2 and PGF2α fell from control values of 286.1±73.7 and 143.5±25.9 pg/min to 31.2±9.9 and 23.6±9 pg/min following 2 mg/kg indomethacin and to 36.8±4.4 and 8.9±1.9 pg/min following 5 mg/kg Ro 20-5720. Reduction of PG excretion was not reversible during the time of the experiment. Our results demonstrate a consistent decrease of tubuloglomerular feedback responses during inhibition of prostaglandin biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581431
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    Paper (German National Licenses)
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