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  • Portland Press Ltd.  (14)
  • 1
    Online Resource
    Online Resource
    Effect of angiotensin II and of an Angiotensin II Analogue (Sar1-Ile8-Angiotensin II) on Blood Pressure, Plasma Aldosterone and Plasma Renin Activity in the Dog
    Portland Press Ltd. ; 1974
    In:  Clinical Science Vol. 48, No. s2 ( 1974-01-01), p. 41s-44s
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 48, No. s2 ( 1974-01-01), p. 41s-44s
    Abstract: 1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not to be related to its vasoconstrictive activity.
    Type of Medium: Online Resource
    ISSN: 0144-4107
    URL: Article
    DOI: 10.1042/cs048041s
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1974
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  • 2
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    Percutaneous Transluminal Dilatation of Renal Artery Stenosis: 2 years' Experience
    Portland Press Ltd. ; 1981
    In:  Clinical Science Vol. 61, No. s7 ( 1981-12-01), p. 481s-483s
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 61, No. s7 ( 1981-12-01), p. 481s-483s
    Abstract: 1. Percutaneous transluminal dilatation was performed in 37 patients with renovascular hypertension: 24 had atherosclerotic renal artery stenosis and 13 had fibromuscular dysplasia. 2. Percutaneous transluminal dilatation could not be performed for technical reasons in three (8%) of the 37 patients. 3. In the remaining 34 patients blood pressure fell significantly (P & lt; 0.001) from 201 ± 31/118 ± 14 mmHg to 144 ± 22/91 ± 11 mmHg 3 days after the procedure. The respective values at months 6 and 24 were 148 ± 26/89 ± 12 mmHg (n = 23, P & lt; 0.001) and 143 ± 14/89 ± 6 mmHg (n = 8, P & lt; 0.001). 4. Certain differences between the two subgroups emerged in the response to percutaneous transluminal dilatation (6 months values, n = 23): cure rate was higher in patients with fibromuscular dysplasia than in those with atherosclerotic stenosis (67% vs 35%) and in contrast to atherosclerotic stenosis none of the cases with fibromuscular dysplasia was unimproved. 5. Follow-up angiography performed at month 6 showed recurrence of slight renal artery stenosis in five out of 19 patients (all atherosclerotic). 6. Complications were seen in six (16%) of the 37 patients. 7. Our results show that percutaneous transluminal dilatation is a valid method for the treatment of renovascular hypertension. Patients with fibromuscular dysplasia may show a better response than those with atherosclerotic stenosis. In this study the latter was complicated by a high risk of developing restenosis. Finally a complication rate of 16% requires careful selection of patients.
    Type of Medium: Online Resource
    ISSN: 0144-9664
    URL: Article
    DOI: 10.1042/cs061481s
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1981
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  • 3
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    Online Resource
    Angiotensin II Binding to Human Mononuclear Cells: Receptor or Free Fluid Endocytosis?
    Portland Press Ltd. ; 1984
    In:  Clinical Science Vol. 66, No. 5 ( 1984-05-01), p. 605-612
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 66, No. 5 ( 1984-05-01), p. 605-612
    Abstract: 1. It has recently been claimed that there are angiotensin II (ANG II) receptors on human mononuclear cells and on platelets and this has been used for investigating the regulation of the renin-angiotensin system in hypertension. We here show the following. 2. Binding kinetics of 125I-labelled ANG II and [3H]ANG II to mononuclear cells were slow (maximum at 90 min) and the same as for [3H] -inulin. 3. As with [3H]inulin there was no binding at 4°C. 4. Release from the cells was slow and incomplete (about 30% after 15 min, 60% after 60 min). 5. Binding was not saturable over a range from 10−12 to 10−6 mol of ANG II/l, about 8% of offered peptide being bound at all concentrations. 6. Various inhibitors of free fluid endocytosis exhibited the same inhibition pattern of ANG II binding to mononuclear cells. 7. Therefore uptake of ANG II into mononuclear cells displayed all the features of free fluid endocytosis. 8. ANG II was degraded by carboxypeptidase A. When this degradation was prevented by d-phenylalanine, no binding occurred. 9. In platelet preparations contaminated by 0.3-5% of mononuclear cells, 125I-labelled ANG II was degraded as well. Free fluid endocytosis of the degradation product strongly depended on the percentage of contaminating mononuclear cells. 10. We conclude that there are no ANG II receptors on human mononuclear cells and that their presence on human platelets is doubtful.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/cs0660605
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1984
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  • 4
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    Online Resource
    Effect of Immunization against Angiotensin II on Blood Pressure and on Plasma Aldosterone in the Rabbit
    Portland Press Ltd. ; 1975
    In:  Clinical Science Vol. 48, No. 5 ( 1975-05-01), p. 413-420
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 48, No. 5 ( 1975-05-01), p. 413-420
    Abstract: 1. Rabbits were actively immunized against angiotensin II (AII). 2. Basal plasma aldosterone concentration was 0.058 ±0.027 pmol/ml (20.7±9.6 pg/ml) (mean±SD) in immunized and 0.056±0.021 pmol/ml (20.2±7.5 pg/ml) in control animals during suppression of adrenocorticotrophic hormone by dexamethasone. When the endogenous formation of AII was stimulated by frusemide, by haemorrhage or by feeding with low sodium diet, a significant increase of plasma aldosterone was observed with no difference between immunized and non-immunized animals. 3. In non-immune rabbits, the average mean arterial blood pressure rose 13 mmHg during the infusion of AII (5 pmol min−1 kg−1) and 27 mmHg during the infusion of 50 pmol min−1 kg−1. In contrast, there was no clear increase in blood pressure in the immunized animals. The blood pressure rose in immune animals (15 mmHg) and in non-immune animals (36 mmHg) during the infusion of 200 pmol min−1 kg−1 AII. Plasma aldosterone rose in all animals in response to each of the three infusions with no significant difference between the two groups. 4. It is concluded that the immunization against AII blocked only the pressor effect of the peptide but had no clear influence on the response of plasma aldosterone to increased AII. Differences between the affinities of the adrenal and vascular AII receptors may explain these findings.
    Type of Medium: Online Resource
    ISSN: 0301-0538
    URL: Article
    DOI: 10.1042/cs0480413
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1975
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  • 5
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    Online Resource
    Studies on the Effect of Angiotensin II and of Des1-angiotensin II on Blood Pressure, Plasma Renin Activity and Plasma Aldosterone in the Dog
    Portland Press Ltd. ; 1976
    In:  Clinical Science Vol. 51, No. s3 ( 1976-01-01), p. 147s-150s
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 51, No. s3 ( 1976-01-01), p. 147s-150s
    Abstract: 1. The effects of infusions of equimolar doses of angiotensin II (AII) and of Des1-angiotensin II (heptapeptide) on plasma renin activity, blood pressure and plasma aldosterone were compared in normal anaesthetized dexamethasone-suppressed dogs. 2. Plasma renin activity was equally suppressed by both compounds. The increase in blood pressure induced by the heptapeptide averaged 43–62% of the increase during AII infusions. No significant differences in aldosterone increase were observed between AII and the heptapeptide. Plasma aldosterone, however, dropped significantly faster in heptapeptide-treated dogs after the end of the infusions. 3. Sar1-Ala8-angiotensin II (saralasin, 400 pmol min—1 kg—1) suppressed plasma aldosterone that was stimulated by heptapeptide (20 pmol min—1 kg—1) completely. The same angiotensin antagonist had only a moderate effect on plasma aldosterone stimulated by AII. After stopping the antagonist infusion, plasma aldosterone rose significantly higher in dogs infused with AII than in those receiving the heptapeptide. 4. The results demonstrate differences between the effects of AII and the heptapeptide both on blood pressure and on plasma aldosterone. They do not support the hypothesis that the heptapeptide may be the main mediator of aldosterone secretion.
    Type of Medium: Online Resource
    ISSN: 0144-4107
    URL: Article
    DOI: 10.1042/cs051147s
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1976
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  • 6
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    Stereospecific modulation of the calcium channel in human erythrocytes by cholesterol and its oxidized derivatives
    Portland Press Ltd. ; 1985
    In:  Biochemical Journal Vol. 227, No. 1 ( 1985-04-01), p. 105-112
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 227, No. 1 ( 1985-04-01), p. 105-112
    Abstract: To study the effect of cholesterol and its pathophysiologically important oxidized derivatives (OSC) on the calcium entry channel, the human red blood cell was used as a model system. The calcium ejecting adenosinetriphosphatase (ATPase) was inhibited by vanadate. The cells were loaded with OSC at concentrations between 1.25 × 10(-5) and 25 × 10(-5) mol/l. 22-Hydroxycholesterol, cholestan-3 beta,5 alpha,6 beta-triol, 5 alpha-cholestan-3 beta-ol,3 beta,5 alpha-dihydroxycholestan-6-one and 3 beta-hydroxy-5 alpha-cholestan-7-one stimulated 45Ca2+ influx by up to almost 90%, whereas 25-hydroxycholesterol, 7 beta-hydroxycholesterol, 20 alpha-hydroxycholesterol and 7-oxocholesterol inhibited influx by up to 75%. Both stimulation and inhibition were dependent on the amount of OSC incorporated into the membrane. More than 90% of the total modification of calcium influx by OSC was accounted for by an influence on the nitrendipine-inhibitable part of influx. Enrichment of cholesterol in the membrane greatly stimulated, and cholesterol depletion inhibited, Ca2+ influx. These results demonstrate that cholesterol and its oxidized derivatives are able to modulate the calcium channel in human red blood cells in a highly stereospecific manner.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj2270105
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1985
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 7
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    Online Resource
    Collagen metabolism in cultured osteoblasts from osteogenesis imperfecta patients
    Portland Press Ltd. ; 1992
    In:  Biochemical Journal Vol. 286, No. 1 ( 1992-08-15), p. 73-77
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 286, No. 1 ( 1992-08-15), p. 73-77
    Abstract: Collagen produced in vitro by bone cells isolated from 19 patients with different forms of osteogenesis imperfecta (OI) was analysed. Clinically, four patients were classified as OI type I, 10 patients as OI type III and five patients as OI type IV. Bone cells of 12 of the 19 OI patients produced structurally abnormal type I collagen. Electrophoretically uniformly slower migrating collagen type I alpha-chains were found in one case of OI type I, in seven cases of OI type III and in one case of OI type IV; two cultures of OI type III produced two different populations of collagen type I alpha-chains, and one culture of OI type IV showed reduction-sensitive dimer formation of alpha 1(I) chains, resulting from the inadequate incorporation of a cysteine residue into the triple helical domain of alpha 1(I). Quantitative analysis of collagen metabolism led to the distinction of two groups of cultured OI osteoblasts. In osteoblasts of OI type I, mainly production of collagen was decreased, whereas secretion, processing and pericellular accumulation of (pro)collagen type I was similar to that in control osteoblasts. In contrast, in osteoblasts of OI types III and IV, production as well as secretion, processing and pericellular accumulation of (pro)collagen type I were significantly decreased. Low levels of type I collagen were found irrespective of the presence or absence of structural abnormalities of collagen type I in all OI types.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj2860073
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1992
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 8
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    Online Resource
    Interleukin-6, but not tumour necrosis factor- α , increases lipogenesis in rat hepatocyte primary cultures
    Portland Press Ltd. ; 1994
    In:  Biochemical Journal Vol. 301, No. 1 ( 1994-07-01), p. 193-197
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 301, No. 1 ( 1994-07-01), p. 193-197
    Abstract: The Kupffer-cell products interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) have been shown to stimulate hepatic lipogenesis in vivo. Studies were performed to define the direct effects of these cytokines on lipogenesis in primary-culture rat hepatocytes. Hepatocytes were cultured in the presence of IL-6 or TNF-alpha for periods of 24-72 h. IL-6 increased hepatocyte protein content per microgram of DNA. IL-6 also caused a dose- and time-dependent induction of hepatocyte capacity for incorporation of [2-14C]pyruvate into fatty acids (56% increase by 12.5 ng/ml IL-6 after 72 h of cytokine exposure). This increase in cellular lipogenic capacity was confirmed by using 3H2O incorporation into fatty acids as tracer. TNF-alpha did not increase hepatocyte lipogenesis. In contrast with studies in vivo, neither IL-6 nor TNF-alpha had any acute (2 h of exposure) effects on rates of lipogenesis. Both IL-6 and TNF-alpha are known to increase macrophage prostaglandin synthesis acutely. The prostaglandin E agonist misoprostol free acid (0.1 microM) acutely increased hepatocyte lipogenic rates by 14%. Thus, IL-6 can directly induce hepatocyte lipogenic capacity, and E-series prostaglandins can antagonize the acute inhibition of lipogenesis by glucagon. The observations provide further evidence for the role of Kupffer-cell products in the regulation of hepatocyte metabolism.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj3010193
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1994
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 9
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    The Trp triad within the V-domain of the receptor for advanced glycation end products modulates folding, stability and ligand binding
    Portland Press Ltd. ; 2020
    In:  Bioscience Reports Vol. 40, No. 1 ( 2020-01-31)
    Details
    In: Bioscience Reports, Portland Press Ltd., Vol. 40, No. 1 ( 2020-01-31)
    Abstract: The receptor for advanced glycation end products (RAGE) recognizes damage-associated molecular patterns (DAMPs) and plays a critical role for the innate immune response and sterile tissue inflammation. RAGE overexpression is associated with diabetic complications, neurodegenerative diseases and certain cancers. Yet, the molecular mechanism of ligand recognition by RAGE is insufficiently understood to rationalize the binding of diverse ligands. The N-terminal V-type Ig-domain of RAGE contains a triad of tryptophan residue; Trp51, Trp61 and Trp72. The role of these three Trp residues for domain folding, stability and binding of the RAGE ligand S100B was investigated through site-directed mutagenesis, UV/VIS, CD and fluorescence spectrometry, protein–protein interaction studies, and X-ray crystallography. The data show that the Trp triad stabilizes the folded V-domain by maintaining a short helix in the structure. Mutation of any Trp residue increases the structural plasticity of the domain. Residues Trp61 and Trp72 are involved in the binding of S100B, yet they are not strictly required for S100B binding. The crystal structure of the RAGE-derived peptide W72 in complex with S100B showed that Trp72 is deeply buried in a hydrophobic depression on the S100B surface. The studies suggest that multiple binding modes between RAGE and S100B exist and point toward a not previously recognized role of the Trp residues for RAGE-ligand binding. The Trp triad of the V-domain appears to be a suitable target for novel RAGE inhibitors, either in the form of monoclonal antibodies targeting this epitope, or small organic molecules.
    Type of Medium: Online Resource
    ISSN: 0144-8463 , 1573-4935
    URL: Article
    DOI: 10.1042/BSR20193360
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2020
    detail.hit.zdb_id: 2014993-1
    SSG: 12
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  • 10
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    Intracellular Na+ and Ca2+ Activities in Essential Hypertension
    Portland Press Ltd. ; 1982
    In:  Clinical Science Vol. 63, No. s8 ( 1982-10-01), p. 41s-43s
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 63, No. s8 ( 1982-10-01), p. 41s-43s
    Abstract: 1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P & lt; 0.01) and 6.63 ± 0.88 mmol/l (P & lt; 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P & lt; 0.05). 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P & lt; 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P & lt; 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P & lt; 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P & lt; 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P & lt; 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l. 4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.
    Type of Medium: Online Resource
    ISSN: 0144-9664
    URL: Article
    DOI: 10.1042/cs063041s
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1982
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