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  • 11
    Electronic Resource
    Electronic Resource
    IN VITRO AUTORADIOGRAPHIC ENDOTHELIN-1 BINDING SITES AND SARAFOTOXIN S6B BINDING SITES IN RAT TISSUES (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The distribution of binding sites for [125I]-labelled endothelin-1 ([125I]-ET-1) and [125I]-labelled sarafotoxin S6B ([125I]-SRT) was visualized in rat tissues using in vitro autoradiography.2. A high density of endothelin-1 (ET-1) binding was found in the heart. In the kidney, ET-1 binding occurred in association with glomeruli, proximal tubules, the inner stripe and inner medulla. In the adrenal, a high density of ET-1 binding occurred in the medulla as well as the zona glomerulosa.3. The binding affinity constant (KA) for ET-1 binding in these sites ranged from 1 to 10 X 109/mol per litre.4. Although sarafotoxin S6B (SRT) was 10–100-fold weaker than ET-1 in displacing [125I]-ET-1 from these sites, 1 μmol/L unlabelled SRT completely abolished [125I]-ET-1 binding in all sites. Other venom peptides did not affect [125I]-ET-1 binding.5. The pattern of [125I]-SRT receptor binding in rat tissues by in vitro autoradiography was identical to that for ET-1 receptor binding, and both unlabelled SRT and unlabelled ET-1 fully competed with [125I]-SRT for binding.6. These results provide evidence that SRT binds to the ET receptor in a range of rat tissues. The results suggest that there may be subclasses of ET receptors which can be distinguished by the relative potencies of ET-1 and SRT at various tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01485.x
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  • 12
    Electronic Resource
    Electronic Resource
    Effect of omeprazole, an inhibitor of H+, K+-ATPase, on bone resorption in humans (1993)
    Springer
    Calcified tissue international 53 (1993), S. 21-25 
    Details
    ISSN: 1432-0827
    Keywords: Omeprazole ; Bone ; Resorption ; Inhibition ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Omeprazole is an inhibitor of gastric H+, K+-ATPase. Although the major proton transport of osteoclast is mediated by a vacuolar-type H+-ATPase which is different from the gastric H+, K+-ATPase,in vitro studies have demonstrated that omeprazole inhibits bone resorption. In this study, the effect of omeprazole on bone resorption was evaluated in patients who had a history of gastric ulcer and were treated with maintenance doses of H2 blocker without any gastric complaints at the study time. H2 blocker administration was changed to omeprazole treatment in the study group and to no treatment in the control group. Urinary excretion of hydroxyproline and calcium decreased after omeprazole treatment in the study group. Serum intact PTH, alkaline phosphatase, osteocalcin, and tartrate-resistant acid phosphatase (TRAP) increased in this group. In the control group, there were not any changes in these parameters. The discrepancy between serum TRAP and urinary excretion of hydroxyproline and calcium in the study group was thought to be due to the suppression of bone resorption by omeprazole, which probably interfered the acidification at resorption lacunae and resulted in the inactivation of TRAP and other lysosomal enzymes. The results of our study suggest the possibility that the specific inhibitors of the osteoclastic proton pump (such as bafilomycins) will more effectively suppress bone resorption and be useful for the treatment of metabolic bone diseases with increased bone resorption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01352010
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  • 13
    Electronic Resource
    Electronic Resource
    The effect of graded calcium infusions on rhythmic blood pressure oscillations in normal man (1995)
    Springer
    Clinical autonomic research 5 (1995), S. 5-11 
    Details
    ISSN: 1619-1560
    Keywords: Calcium ; Blood pressure oscillations ; Power spectrum ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was designed to determine whether calcium contributes to the regulation of rhythmic oscillations in blood pressure. Six normal subjects received sequential 1-h infusions of calcium gluconate (1.5, 3.0 and 4.5 mg calcium/kg/h) during continuous blood pressure (Finapres) monitoring. The plasma ionized calcium ([Ca2+]) concentration increased from 4.6 ± 0.07 mg/dl to 5.97 ± 0.20 mg/dl (p 〈 0.01) with infusion. The mid-frequency (0.07-0.14 Hz, Mayer wave) power spectrum of diastolic blood pressure was depressed slightly following the first dose but increased significantly following the final dose (p 〈 0.05). The high-frequency (0.15–0.40 Hz) power spectrum of systolic blood pressure decreased following the first dose (p 〈 0.05) and subsequently remained low. The low-frequency (0.02–0.06 Hz) power spectrum was not affected. These results demonstrate that graded hypercalcaemia affects blood pressure oscillations in man. Our data suggest that the amplitude of the Mayer wave, a clinical marker of sympathetic vascular tone, is modulated in part by calcium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01845492
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  • 14
    Electronic Resource
    Electronic Resource
    Effects of cicletanine on the urinary excretion of prostanoids and kallikrein, and on renal function in man (1993)
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 253-256 
    Details
    ISSN: 1573-7241
    Keywords: cicletanine ; prostacyclin ; thromboxane ; natriuresis ; kallikrein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of cicletanine, a new antihypertensive agent, on the prostaglandin-kallikrein system and the reninangiotensin system were studied. A single oral dose of 200 mg cicletanine or placebo was administered to 9 healthy male volunteers, with samples of blood and urine obtained before and 2 hours after drug administration. Cicletanine increased the urine flow, urinary excretion of sodium, and fractional excretion of sodium by 47%, 115%, and 104%, respectively. While the excretion of 6-keto-prostaglandin-F1α was enhanced significantly, urinary excretion of thromboxane-B2, prostaglandin-E2, and kallikrein were unchanged. Cicletanine also did not alter plasma renin activity, plasma aldosterone concentration, or creatinine clearance. These observations suggest that cicletanine may suppress sodium reabsorption at the nephron, and it may stimulate prostacyclin generation with no effect on that of thromboxane-A2. Thus cicletanine may be beneficial in the management of cardiovascular disorders in which the equilibrium between prostacyclin and thromboxane is disturbed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00878515
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