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  • 1
    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
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 253 (1966), S. 65-65 
    ISSN: 1432-1912
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Nitric oxide ; NG-nitro-L-arginine methyl ester ; Kidney ; Heart ; Hypertension ; Renal haemodynamics ; Renin-angiotensin system ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inhibition of the angiotensin converting enzyme (ACE) with ramipril was studied in male Wistar rats during long-term inhibition of nitric oxide (NO) synthase by NG-nitro-l-arginine methyl ester (l-NAME). Chronic treatment with l-NAME in a dose of 25 mg/kg per day over 6 weeks caused myocardial hypertrophy and a significant increase in systolic blood pressure (245 ± 16 mmHg) as compared to controls (155+4 mmHg). Animals receiving simultaneously l-NAME and ramipril were protected against blood pressure increase and partially against myocardial hypertrophy. L-NAME caused a significant reduction in glomerular filtration rate (GFR: 2.56+0.73 ml·kg−1·min−1) and renal plasma flow (RPF: 6.93±1.70ml·kg−1·min−1) as compared to control (GFR: 7.29±0.69, RPF: 21.36±2.33ml·kg−1·min−1). Addition of ramipril prevented l-NAME-induced reduction in GFR and renal plasma flow. l-NAME produced an elevation in urinary protein excretion and serum creatinine and a decrease in potassium excretion which was antagonised by ramipril. L-NAME-induced increase in plasma renin activity (PRA) was further elevated with ramipril treatment. Isolated hearts from rats treated with l-NAME showed increased post-ischaemic reperfusion injuries. Compared to controls duration of ventricular fibrillation was increased and coronary flow reduced. During ischaemia the cytosolic enzymes lactate dehydrogenase and creatine kinase, as well as lactate in the venous effluent were increased. Myocardial tissue values of glycogen, ATP, and creatine phosphate were decreased, whereas lactate was increased. Coadministration of ramipril reversed these effects. l-NAME treatment reduced the cyclic GMP content in urine and renal arteries, and was not changed by additional ramipril-treatment. In the kidney hyalinosis of arterioles and of glomerular capillaries, as well as mesangial expansion and tubular atrophies seen after long-term inhibition of NO synthase were reduced by coadministration of ramipril. In conclusion, long-term ACE inhibition by ramipril prevented l-NAME-induced hypertension and cardiac hypertrophy, and attenuated functional and morphological changes in the kidneys. In addition, cardiac-dynamic and -metabolic deterioration induced by L-NAME was normalised by co-treatment with ramipril.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 44 (1966), S. 1297-1300 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 1 mg Glucagon administered intravenously raised the blood glucose level in 9 out of 12 healthy subjects by more than 30 mg-% and in all cases the plasma catecholamine level by 35–185% between 5–20 min after injection. After Reserpine pretreatment with 12 mg daily over a five day period in 6 patients with psychic disorders the hyperglycemic and catecholamine liberating action of glucagon was diminished in 4 cases. Despite a twofold to threefold increase in the catechol amine plasma level, the blood pressure and the pulse rate remained within the norm. The noradrenaline sensitivity in 10 out of 11 healthy subjects was decreased after administration of 1 mg glucagon. The amount of noradrenaline necessary for a 20 mm Hg rise in the diastolic blood pressure was 23–89% higher than in the control without glucagon. Therefor glucagon is assumed to have an adrenergic blocking action. The physiological significance of a catecholamine release as part of the glucagon action is discussed.
    Notes: Zusammenfassung Intravenöse Injektion von 1 mg Glucagon führte bei neun von zwölf gesunden Versuchspersonen zu einem Blutzuckeranstieg um mehr als 30 mg-% und in allen Fällen zu einer deutlichen Erhöhung des Katecholamin-Plasmaspiegels um maximal 33–185% des Ausgangswertes zwischen 5 und 20 min nach der Injektion. Eine Dosis von 0,1 mg Glucagon war ebenfalls wirksam. Nach fünftägiger Vorbehandlung mit täglich 12 mg Reserpin bei sechs psychisch Kranken waren die hyperglykämische und die Katecholamin freisetzende Glucagonwirkung bei den vier Patienten, welche sediert waren, vermindert. Blutdruck und Pulsfrequenz blieben trotz Steigerung des Katecholamin-Plasmaspiegels im Bereich normaler Spontanschwankungen. Nach der gleichen Dosis Glucagon war die Noradrenalin-Empfindlichkeit bei zehn von elf Versuchspersonen vermindert, die zur diastolischen Drucksteigerung um 20 mm Hg erforderliche Dosis um 23–89% erhöht. Dies wird als Ausdruck einer adrenergisch blockierenden Glucagonwirkung angesehen. Die Bedeutung der Befunde für die physiologische Glucagonwirkung wird diskutiert.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2013
    Keywords: Key wordsKATP channel ; Cardiomyocytes ; Anoxia ; Glibenclamide ; Fura-2 ; Hypoxic shortening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the temporal relationship between the adenosine triphosphate-sensitive K current (K ATP current), hypoxic shortening and Ca accumulation in cardiomyocytes exposed to anoxia or metabolic inhibition. Whole-cell, patch-clamp experiments were performed with nonstimulated isolated rat heart ventricular muscle cells loaded with the Ca-sensitive fluorescent dye 1-[2-(5-carboxyoxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2′-amino-5′-methylphenoxy) ethane-N,N,N′,N′-tetraacetic acid (fura-2) via the patch pipette. After approximately 8 min anoxia, the K ATP current started to rise and reached a maximum of 21.3 ± 3.7 nA (n = 5, recorded at 0 mV clamp potential) within 1–3 min. At that time hypoxic contracture also occurred. Resting cytoplasmic free calcium (Cai) did not change significantly before hypoxic shortening. After hypoxic contracture, the K ATP current decreased and Cai started to rise, reaching about 1 μmol/l. The presence of glibenclamide (10 μmol/l) in the bath reduced the anoxia-induced K ATP current by more than 50%, but did not significantly influence the time dependence of current, hypoxic shortening and Cai, or the magnitude of Cai. Metabolic inhibition with 1.5 mmol/l CN resulted in K ATP current increase and hypoxic shortening, occurring somewhat earlier than under anoxia, but all other parameters were comparable. In non-patch-clamped cells loaded with fura-2 AM ester and field-stimulated with 1 Hz, 1 μmol/l glibenclamide had no significant effect on the magnitude of the Cai increase caused by exposure of the cells to 1.5 mmol/l CN−. After CN− wash-out in non-patch-clamped cells, Cai declined, oscillated and finally returned to control values. It can be concluded that glibenclamide inhibits anoxia-induced K ATP currents only partially and has no significant effect on anoxia-induced rise in resting Cai.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2013
    Keywords: Cell volume ; Intracellular pH ; ras oncogene ; Calcium oscillations ; Cell membrane potential ; Bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ras) bradykinin leads to sustained oscillations of cell membrane potential due to oscillations of intracellular Ca2+ with subsequent activation of Ca2+-sensitive K+ channels. In cells not expressing the oncogene (-ras), bradykinin leads only to a single transient hyperpolarization of the cell membrane. The present study has been performed to elucidate the possible interaction of cell volume, intracellular pH and bradykinin-induced oscillations of the cell membrane potential. Bradykinin leads to cell shrinkage and intracellular alkalinization of both +ras cells and −ras cells. Inhibition of Na+/H+ exchanger by HOE 694 abolishes the bradykinin-induced alkalinization but does not significantly interfere with the bradykinin-induced oscillations of cell membrane potential. In contrast, prevention of bradykinin-induced cell shrinkage by simultaneous reduction of extracellular osmolarity blunts the oscillations. Thus, cell shrinkage stimulates bradykinin-induced oscillations of cell membrane potential. On the other hand, cell shrinkage alone does not elicit oscillations unless, in addition, Ca2+ entry is stimulated by ionomycin.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1435-1803
    Keywords: Key words Aortocaval shunt – angiotensin receptor – mRNA – heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the regulation of the angiotensin receptor type 1 (AT1) in different organs in cardiac volume overload, we measured AT1 mRNA content in the atria, left and right ventricle, kidney and liver of rats with an aortocaval shunt, produced by infrarenal aortocaval puncture 4 weeks earlier. For angiotensin receptor mRNA quantitation a novel quantitative PCR procedure based on liquid phase hybridization was used that allowed the determination of absolute AT1 mRNA copy numbers and its comparison in different organs. Glyceraldehydephosphate dehydrogenase (GAPDH) mRNA was measured by RT-PCR to control externally equal mRNA content and quality of RNA extraction in shunt animals and controls. Heart weight was increased in the shunt animals, with the greatest increase in the atria. Blood pressure, plasma renin activity, plasma angiotensin I and II and aldosterone concentrations were not significantly altered. The AT1 mRNA content was significantly increased in the atria (shunt: 1167 ± 350 copies AT1 mRNA/ng RNA vs controls: 803 ± 240; p 〈 0.05). No change was found in the right or left ventricle, in the kidney and liver. The findings document that atrial hypertrophy in cardiac volume overload parallel with a significant increase in atrial AT1 mRNA content.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-1803
    Keywords: isolated dog heart ; collateral circulation ; Prostacyclin ; Adenosine ; radioactive microspheres ; myocardial blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dogs were subjected to chronic occlusion of the left circumflex and the right coronary artery by ameroid-type constrictors 4–5 weeks before the experiments. The hearts were isolated, fibrillated and perfused with blood (100 mmHg) from a support dog. Total and regional myocardial blood flow as well as peripheral coronary pressure (circumflex artery) were determined before and during infusion of PGI2 and ASN into the isolated hearts. Both drugs increased total and regional blood flow to all parts of the myocardium in a dose-dependent manner, PGI2 being 2–3 times more potent than ASN. The perfusion pressure for the collateral-dependent myocardium, the peripheral coronary pressure, decreased following high doses of both drugs. For PGI2 a dose level existed where total flow was increased, while peripheral coronary pressure remained unaffected. After termination of the infusion of PGI2, peripheral coronary pressure rose above predrug level with the total blood flow still being elevated. These findings indicate a PGI2-induced dilatation of collateral vessels. In general, the hemodynamic profile within the isolated hearts and the support dogs was characterized by the pronounced vasodilatory effects of PGI2 on arterioles. However, these effects did not deteriorate further the nonhomogenous blood flow distribution in the collateralized portions of the myocardium. The findings suggest that PGI2 is not a specific coronary vasodilator.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 86 (1991), S. 293-296 
    ISSN: 1435-1803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1435-1803
    Keywords: Aortocaval shunt ; angiotensin receptor ; mRNA ; heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the regulation of the angiotensin receptor type 1 (AT1) in different organs in cardiac volume overload, we measured AT1 mRNA content in the atria, left and right ventricle, kidney and liver of rats with an aortocaval shunt, produced by infrarenal aortocaval puncture 4 weeks earlier. For angiotensin receptor mRNA quantitation a novel quantitative PCR procedure based on liquid phase hybridization was used that allowed the determination of absolute AT1 mRNA copy numbers and its comparison in different organs. Glyceraldehydephosphate dehydrogenase (GAPDH) mRNA was measured by RT-PCR to control externally equal mRNA content and quality of RNA extraction in shunt animals and controls. Heart weight was increased in the shunt animals, with the greatest increase in the atria. Blood pressure, plasma renin activity, plasma angiotensin I and II and aldosterone concentrations were not significantly altered. The AT1 mRNA content was significantly increased in the atria (shunt: 1167±350 copies AT1 mRNA/ng RNA vs controls: 803±240; p〈0.05). No change was found in the right or left ventricle, in the kidney and liver. The findings document that atrial hypertrophy in cardiac volume overload parallel with a significant increase in atrial AT1 mRNA content.
    Type of Medium: Electronic Resource
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