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  • Cushing's syndrome  (4)
  • phospholamban  (4)
  • Springer  (8)
  • 1
    Electronic Resource
    Electronic Resource
    Captopril in Cushing's syndrome (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 855-858 
    Details
    ISSN: 1432-1440
    Keywords: Cushing's syndrome ; Pathogenesis of hypertension ; Renin angiotensin system ; Captopril
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To analyse the role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome ten patients with hypercorticism (five with pituitary hypothalamic dysfunction, three with adrenal adenomas and two with adrenal carcinomas) received a single oral dose of 25 mg captopril. Mean arterial pressure was then determined at short intervals over periods of up to 240 min. Plasma renin activity (PRA) was measured immediately before the administration of captopril. Eleven patients with severe essential hypertension, who showed a comparable distribution of basal PRA values, served as a control. Patients with elevated basal PRA values (〉3 ng/ml·3 h) showed, both in the subgroup of cases with essential hypertension and in that with Cushing's syndrome, a statistically significant fall (P〈0.05−P〈0.001) in mean arterial pressure, the decrease being slightly more pronounced in essential hypertensives. On the other hand patients with normal PRA values (≦3 ng/ml·3 h) exhibited only a minor fall in mean arterial pressure reaching statistical significance (P〈0.05) only after 60 min (essential hypertension) and 180 min (Cushing's syndrome), respectively. Our results document that in patients with Cushing's syndrome the effect of captopril seems to be determined by the activity of the renin angiotensin system. Thus, in a substantial number of patients with hypercorticism, the renin angiotensin system may be an important factor in the pathogenesis of hypertension, whereas in patients with low PRA values other factors like oversecretion of mineralocorticoids may be responsible for the observed blood pressure increases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01712002
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  • 2
    Electronic Resource
    Electronic Resource
    The effect of saralasin (1-Sar-8-Ala-Angiotensin II) on blood pressure in patients with cushing's syndrome (1976)
    Springer
    Journal of molecular medicine 54 (1976), S. 661-663 
    Details
    ISSN: 1432-1440
    Keywords: Cushing-Syndrom ; Hypertonie ; Renin-Aktivität ; Aldosteronismus ; Cushing's syndrome ; Hypertension ; Renin activity ; Aldosteronism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary To investigate the role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome two patients with hypercorticism were infused with 20 mg saralasin (1-sar-8-alaangiotensin II) over a period of 30 minutes under constant blood pressure control. In addition, one patient with primary aldosteronism, an established form of mineralocorticoid hypertension, served as control. Neither in the two patients with Cushing's syndrome nor in the patient with primary aldosteronism could a blood pressure lowering effect of saralasin be observed. In the two patients with hypercorticism both renin activity and plasma aldosterone increased during saralasin infusion. The patient with primary aldosteronism only showed a weak increase in plasma aldosterone concentration. These results seem to exclude an important role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome. The unresponsiveness of elevated blood pressure to saralasin in the two patients with hypercorticism and in the patient with primary aldosteronism indirectly supports the assumption that in patients with Cushing's syndrome increased mineralocorticoid activity may be the main factor in the pathogenesis of hypertension.
    Notes: Zusammenfassung Um die Bedeutung des Renin-Angiotensin Systems in der Pathogenese der Hypertonie bei Cushing-Syndrom zu untersuchen, wurden bei 2 Patienten mit Hyperkortizismus 20 mg Saralasin (1-Sar-8-Ala-Angiotensin II) über einen Zeitraum von 30 min unter ständiger Blutdruckkontrolle infundiert. Zusätzlich diente ein Patient mit primärem Aldosteronismus, einer etablierten Form von Mineralokortikoidhochdruck, als Kontrolle. Weder bei den 2 Patienten mit Cushing-Syndrom noch bei dem Patienten mit primärem Aldosteronismus ließ sich ein blutdrucksenkender Effekt des Saralasins nachweisen. Die beiden Patienten mit Hyperkortizismus zeigten unter Saralasin sowohl einen Anstieg der Renin-Aktivität als auch des Plasmaaldosterons. Bei dem Patienten mit primärem Aldosteronismus ließ sich nur ein geringgradiger Anstieg der Plasmaaldosteronkonzentration nachweisen. Diese Ergebnisse sprechen gegen eine wichtige Rolle des Renin-Angiotensin Systems in der Pathogenese der Hypertonie bei Cushing-Syndrom. Die Unbeeinflußbarkeit des Hochdrucks durch Saralasin bei den beiden Patienten mit Hyperkortizismus und dem Patienten mit primärem Aldosteronismus stützen indirekt die Annahme, daß bei Patienten mit Cushing-Syndrom eine erhöhte Mineralokortikoidaktivität der Hauptfaktor in der Pathogenese der Hypertonie ist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01469145
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  • 3
    Electronic Resource
    Electronic Resource
    Episodische Cortisolsekretion bei Cusing-Syndrom (1973)
    Springer
    Journal of molecular medicine 51 (1973), S. 1025-1026 
    Details
    ISSN: 1432-1440
    Keywords: Cushing's syndrome ; hydrocortison ; circadian rhythm ; Cushing-Syndrom ; Cortisol ; Tagesrhythmus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Wiederholte ambulante Plasmacortisolbestimmungen bei einer Patientin mit deutlichen klinischen Zeichen des Hyperkortizismus ergaben mit 16–24 µg/100 ml normale Werte. Erst ein unter standardisierten Bedingungen erstelltes Plasmacortisol-Tagesprofil erbrachte den eindeutigen Nachweis der Hypercortisolämie. Im Vergleich zu gesunden Normalpersonen liegen die Plasmacortisolspiegel der Cushing-Patientin auf einer höheren Ebene. Die physiologischen Phasen ruhender Cortisolsekretion in den Abend- und Nachtstunden fehlen. Wie bei Gesunden können wir bei diesem Fall von Hypercortic ismus, beruhend auf bilateraler Nebennierenrinden-Hyperplasie, große Schwankungen des Plasmacortisolspiegels beobachten. Der Wert wiederholter Plasmacortisolbestimmungen in der Abklärung des Cushing-Syndroms wird diskutiert.
    Notes: Summary In a patient with typical features of Cushing's disease, repeated ambulant determinations of plasma cortisol showed normal values with 16 to 24 µg/100 ml. The entire analysis of the circadian variations of plasma cortisol under standardized conditions led to the diagnosis of hypercorticism. Compared with 2 healthy subjects the patient's curve is set at a higher level. Physiological, quiet periods of cortisol secretion in late day-time do not occur. In accord to the normal, we find great variations of plasma cortisol in this case of Cushing's syndrome due to bilateral adrenal hyperplasia. The diagnostic value of plasma cortisol determinations at short term intervals in differentiating the various forms of hypercorticism is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01468296
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  • 4
    Electronic Resource
    Electronic Resource
    Urinary free cortisol versus 17-hydroxycorticosteroids a comparative study of their diagnostic value in Cushing's syndrome (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 545-548 
    Details
    ISSN: 1432-1440
    Keywords: Cushing's syndrome ; Urinary corticosteroids ; diagnosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We evaluated the usefulness of the basal urinary 24-h excretion rates of free cortisol versus 17-hydroxycorticosteroids in the diagnosis of Cushing's syndrome. On an outpatient basis, both urinary free cortisol and 17-hydroxycorticosteroids levels were determined in 48 patients with Cushing's syndrome, as well as in 95 obese and 94 healthy control persons of normal weight. Determination of the urinary free cortisol content allowed a clear-cut distinction between the patients with hypercortisolism and the controls, resulting in a sensitivity of 100% and specificity of 98% for the diagnosis of Cushing's syndrome. The diagnostic accuracy of urinary free cortisol was distinctly superior to that of 17-hydroxycorticosteroids, which showed a wide overlap of values between the groups, with a sensitivity of 73% and a specificity of 94%. In conclusion, the measurement of basal urinary free cortisol provided an excellent diagnostic sensitivity and specificity in the assessment of adrenocortical function. This simple and accurate test thus seems to be particularly useful in the outpatient evaluation of patients with suspected Cushing's syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184788
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  • 5
    Electronic Resource
    Electronic Resource
    Comparative analysis of phospholamban phosphorylation in crude membranes of vertebrate hearts (1985)
    Springer
    Cellular and molecular life sciences 41 (1985), S. 1052-1054 
    Details
    ISSN: 1420-9071
    Keywords: Cardiac muscle ; phylogenesis ; sarcoplasmic reticulum ; phospholamban ; protein kinase ; Ca2+-transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Phospholamban, a sarcoplasmic reticulum phosphoprotein, is present in the hearts of mammalian, avian, amphibian, and fish species. Phylogenetic changes are indicated by marked differences among species in cardiac phospholamban content and by the absence of Ca2+/calmodulin-dependent phospholamban phosphorylation at an early developmental stage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01952139
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  • 6
    Electronic Resource
    Electronic Resource
    Influence of different culture conditions on sarcoplasmic reticular calcium transport in isolated neonatal rat cardiomyocytes (1998)
    Springer
    Molecular and cellular biochemistry 188 (1998), S. 177-185 
    Details
    ISSN: 1573-4919
    Keywords: neonatal rat cardiomyocyte culture ; sarcoplasmic reticulum ; phospholamban ; calcium ATPase ; calcium transport ; thyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract This study investigates sarcoplasmic reticulum (SR) calcium-(Ca2+) transport ATPase (SERCA2a) and phospholamban (PLB) in cultured spontaneously contracting neonatal rat cardiomyocytes (CM) to ascertain the function of both SR proteins under various culture conditions. The two major SR proteins were readily detectable in cultured CM by immunofluorescent microscopy using specific anti-SERCA2 and anti-PLB antibodies. Double labeling technique revealed that PLB-positive CM also labeled with anti-SERCA2. Coexpression of SERCA2 and PLB in CM was supported by measurement of cell homogenate oxalate-supported Ca2+ uptake which was completely inhibited by thapsigargin and stimulated by protein kinase A-catalyzed phosphorylation. Under serum-free conditions, incubation of CM with the SERCA2a expression modulator 3,3′,5-triiodo-L-thyronine (100 nM, 72 h) resulted in elevated Ca2+ uptake of +33%. Specific Ca2+ uptake activity was not altered if insulin was omitted from the serum-free culture medium but total SR Ca2+ transport activity was reduced under this culture condition. The results indicate that primary culture of spontaneously contracting neonatal rat CM can be employed as a useful model system for investigating both short- and long-term mechanisms determining the Ca2+ re-uptake function of the SR under defined culture conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006850724830
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  • 7
    Electronic Resource
    Electronic Resource
    Early postnatal changes in sarcoplasmic reticulum calcium transport function in spontaneously hypertensive rats (1996)
    Springer
    Molecular and cellular biochemistry 163-164 (1996), S. 57-66 
    Details
    ISSN: 1573-4919
    Keywords: heart ; postnatal development ; sarcoplasmic reticulum ; phospholamban ; calcium transport ; spontaneously hypertensive rats ; growth
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract This comparative study investigates the relationship between sarcoplasmic reticulum (SR) calcium(Ca2+)-ATPase transport activity and phospholamban (PLB) phosphorylation in whole cardiac homogenates of spo`ntaneously hypertensive rats (SHR) and their parent, normotensive Wistar Kyoto (WKY) strain during early postnatal development at days 1, 3, 6, 12 and at day 40 to ascertain any difference in SR Ca2+ handling before the onset of hypertension. At day 1, the rate of homogenate oxalate-supported Ca2+ uptake was significantly higher in SHR than in WKY (0.25 ± 0.02 vs 0.12 ± 0.01 nmoles Ca2+/mg wet ventricular weight/min, respectively; p 〈 0.001). This interstrain difference disappeared with further developmental increase in SR Ca2+ transport. Western Blot analysis and a semiquantitative ELISA did not reveal any difference in the amount of immunoreactive PLB (per mg of total tissue protein) between strains at any of the ages studied. In addition, levels of phosphorylated PLB formed in vitro in the presence of radiolabelled ATP and catalytic (C) subunit of protein kinase A did not differ between SHR and WKY at days 1, 3, 6 and 12. At day 40, C subunit-catalyzed formation of 32P-PLB was reduced by 66% (p 〈 0.001) in SHR when compared to age-matched WKY In the early postnatal period between day 1 and 12 SR Ca2+-transport values were linearly related to the respective 32P-PLB levels of both SHR and WKY rats. The results indicate that cardiac SR of SHR can sequester Ca2+ at a much higher rate immediately after birth compared to WKY rats. The disappearance of this interstrain difference with further development suggests that some endogenous neuroendocrine or nutritional factor(s) from the hypertensive mother may exert an influence upon the developing heart in utero resulting in a transiently advanced maturation of the SR Ca2+ transport function in SHR pups at the time of birth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408641
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  • 8
    Electronic Resource
    Electronic Resource
    Mechanisms of thyroid hormone control over sensitivity and maximal contractile responsiveness to β-adrenergic agonists in atria (1998)
    Springer
    Molecular and cellular biochemistry 184 (1998), S. 419-426 
    Details
    ISSN: 1573-4919
    Keywords: atria ; thyroid hormones ; β-adrenergic effect ; sarcoplasmic reticulum ; phospholamban
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract This paper discusses the mechanisms of two basic effects of thyroid hormones on atrial responses to β-adrenergic agonists, i.e. increased inotropic sensitivity and decreased maximal contractile responsiveness. The increased sensitivity of atria to β-adrenergic agonists under thyroid hormones appears to be related to increases in β-adrenoceptor density and Gs/Gi protein ratio, leading to activation of Gs-mediated pathway, but suppression of Gi-mediated pathway of adenylate cyclase regulation. Therefore, the i/c concentrations of cAMP and corresponding inotropic responses achieve their maximums at lower doses of β-adrenergic agonist. Thyroid hormones also decrease the expression of phospholamban, but increase the expression of sarcoplasmic reticulum Ca+2-pump. As a result, the basal activity of sarcoplasmic reticulum Ca+2-pump increases, but its β-adrenergic activation through phosphorylation of phospholamban decreases. It is suggested that these changes are causal for decreased maximal inotropic and lusitropic responses of atria to β-adrenergic agonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006835213108
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