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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 288 (1975), S. 381-402 
    ISSN: 1432-1912
    Keywords: Vasodilator Drugs ; Antihypertensive Drugs ; Excitation-contraction Coupling ; 45Calcium Uptake ; Cyclic AMP ; Lanthanum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Sodium nitroprusside is a potent relaxant of smooth muscles with a predominantly tonic response, e.g. rat aorta contracted by noradrenaline angiotensin II, Phe2-Lys8-vasopressin, BaCl2, or KCl, and guinea-pig tracheal smooth muscle contracted by carbachol. 2. Smooth muscle preparations from the splanchnic region and with varying degrees of phasic contractility are less sensitive and develop tachyphylaxis (portal vein, duodenum of the rat) or are unresponsive to sodium nitroprusside (vas deferens, uterus of the rat). 3. Cardiac auricles of the guinea pig are not affected by sodium nitroprusside in either frequency or amplitude of spontaneous contractions. 4. Sodium nitroprusside causes a parallel shift of the dose-response curve of rat aorta to noradrenaline to the right and reduces the maximum response. 5. The drug has no blocking or stimulant effect on α-or β-adrenoceptors, respectively. 6. Sodium nitroprusside inhibits the contractile response of calcium-depleted depolarized rat aorta to extra-cellular calcium. Like verapamil, it inhibits the increment in 45calcium uptake of rabbit aorta elicited by K+. Sodium nitroprusside significantly reduces 45calcium binding by microsomes prepared from rabbit aorta. 7. Rabbit aorta was incubated with lanthanum chloride to prevent calcium influx; sodium nitroprusside reduced the maintained rapid contraction phase in response to noradrenaline which is believed to be based on the intracellular activation of calcium. 8. In rat aorta, cellular cAMP and ATP levels were not found to be affected by the drug. 9. Rabbit aorta, “skinned” by glycerination, is unresponsive to sodium nitroprusside. 10. It is concluded that sodium nitroprusside acts on excitation-contraction coupling predominantly in tonic smooth muscle by interfering with both the influx and the intracellular activation of calcium.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Hyperparathyroidism ; Glomerular filtration rate ; Urinary cyclic AMP ; Serum parathyroid hormone ; Cyclic AMP ; urinary ; Competitive protein binding assay ; Parathyroid hormone ; Radioimmunoassay ; GFR ; Phosphate excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Urinary cyclic AMP excretion per 24 h or per g creatinine in primary hyperparathyroidism (1° HPT) has been evaluated by several authors with conflicting results. In 50 patients with 1° HPT, 25 patients with secondary (2°) HPT and 35 healthy control persons we determined urinary cyclic AMP per 24 h or per g creatinine. These parameters did not satisfactorily discriminate patients from controls, especially when glomerular filtration rate (GFR) as determined by creatinine clearance was reduced. Since urinary cyclic AMP is derived from plasma by glomerular filtration and from kidney by tubular production—the amount of tubules is reflected by GFR—the cyclic nucleotide was related to GFR. In controls urinary cyclic AMP correlated better with GFR than with creatinine excretion. Additionally, in 45 of 50 patients with 1° HPT and in all with 2° HPT, urinary cyclic AMP/GFR was raised. In 1° HPT serum levels of parathyroid hormone correlated closer with urinary cyclic AMP/GFR than with urinary cyclic AMP/g creatinine. The ratio cyclic AMP/GFR decreased to normal or subnormal values after removal of adenomatous or hyperplastic glands in 1° HPT and during infusion of calcium in 2° HPT. In 50 patients with renal lithiasis caused by diseases other than 1° HPT (anatomical variations, pyelonephritis, immobilization after tetraplegia) the ratio cyclic AMP/GFR was not raised. Urinary cyclic AMP/GFR, therefore, reflects parathyroid hormone excess more reliably than cyclic AMP/g creatinine.
    Notes: Zusammenfassung Parathormon erhöht die renale Ausscheidung von cyclischem AMP (cAMP). Die renale Ausscheidung von cAMP/24 h oder cAMP/g Kreatinin wurde bei primärem Hyperparathyreoidismus (1° HPT) von verschiedenen Untersuchern gemessen. Die Resultate waren widersprüchlich. Wir bestimmten die renale Ausscheidung von cAMP/24 h oder cAMP/g Kreatinin bei 50 Patienten mit 1° HPT, 25 Patienten mit sekundärem (2°) HPT und 35 Kontrollpersonen. Die Patienten schieden im Mittel mehr cAMP/24 h oder cAMP/g Kreatinin aus als die Kontrollpersonen. Eine Überlappung mit dem Normalbereich wurde besonders bei reduzierter Kreatininclearance beobachtet. Da im Urin ausgeschiedenes cAMP zum Teil aus dem Plasma (glomeruläre Filtration) und zum Teil aus der Niere (tubuläre Produktion) stammt und die Anzahl der Tubuli von der GFR reflektiert wird, bezogen wir die renale Ausscheidung von cAMP auf die GFR (bestimmt als Kreatininclearance). Bei den Kontrollpersonen korrelierte die renale Ausscheidung von cAMP besser mit der Kreatininclearance als mit der Kreatininausscheidung. 45 von 50 Patienten mit 1° HPT und alle Patienten mit 2° HPT wiesen eine erhöhte renale Ausscheidung von cAMP/GFR auf. Die radioimmunologisch gemessenen Serumspiegel von Parathormon korrelierten bei 1° HPT besser mit der renalen Ausscheidung von cAMP/GFR als mit cAMP/g Kreatinin. Nach Entfernung von adenomatösen oder hyperplastischen Nebenschilddrüsen bei 1° HPT oder nach Infusion von Calcium bei 2° HPT fiel die Ausscheidung von cAMP/GFR auf normale oder erniedrigte Werte. 50 zusätzlich untersuchte Patienten mit Nephrolithiasis, die nicht durch 1° HPT bedingt war, wiesen keine Erhöhung der renalen Ausscheidung von cAMP/GFR auf. Die renale Ausscheidung von cAMP/GFR ist ein zuverlässigerer Indikator der Nebenschilddrüsenüberfunktion als die Ausscheidung von cAMP/Kreatinin.
    Type of Medium: Electronic Resource
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