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Biomedical subjects

K Hermann

Publications and source records attributed to K Hermann.

At least 55 records · Page 3Linked to original sources
PubMed1994

Increased urinary excretion of angiotensin during anaphylactoid reactions.

Immunoreactive angiotensin I (ANG I) and angiotensin II (ANG II) were measured in human urine, after purification on octadecasilyl-silica cartridges. The total daily excretion of ANG I and II in healthy volunteers was 292.2 +/- 62.5 and 12.2 +/- 2.5 pmol/24 h (mean +/- SEM; n = 14). No differences in the concentrations of ANG I or II were detected between females and males. Although lower levels of ANG I and II were found during the nighttime, no clear-cut circadian rhythm in the excretion of the peptides was found. ANG II was not degraded in acidified urine which shows the effective inhibition of ANG-II-degrading enzymes. Oral provocation tests (OPT) in patients with a history of anaphylactoid reactions (AR) to drugs, foods and food additives were associated with elevated ANG I and II concentrations when symptoms of anaphylaxis occurred. The excretion of ANG I increased by a factor of 7.8 +/- 2.4 and the excretion of ANG II by a factor of 6.1 +/- 1.6 (mean +/- SEM; n = 15). In patients with negative OPT and no clinical symptoms of anaphylaxis, the levels of ANG I and II remained unchanged (n = 26). It is concluded that angiotensin peptides play a role during the events of AR. The peptides may be considered as counteracting factors which stabilize cardiovascular functions.

Adolescent↗
PubMed1994

Histamine, tryptase, norepinephrine, angiotensinogen, angiotensin-converting enzyme, angiotensin I and II in plasma of patients with hymenoptera venom anaphylaxis.

Markers of immediate-type hypersensitivity such as histamine and tryptase were measured in the plasma of nonallergic volunteers and patients with a history of hymenoptera venom anaphylaxis. No significant differences in histamine or tryptase were found between patients and controls. Norepinephrine, an important compound involved in the control of cardiovascular functions and blood pressure, was the same in patients and nonallergic volunteers. In addition, components of the renin-angiotensin system were determined. Patients with hymenoptera venom anaphylaxis showed significantly lower plasma angiotensinogen concentrations as compared to healthy nonallergic controls (p < 0.007), whereas plasma ACE activity was the same. Likewise, the plasma levels of angiotensin I and angiotensin II were significantly reduced in patients as compared to controls (p < 0.04 and p < 0.003, respectively). These findings suggest that the renin-angiotensin system may play an important role as a counteracting factor in hymenoptera venom anaphylaxis.

Adult↗
PubMed1993

Plasma concentrations of arginine vasopressin, oxytocin and angiotensin in patients with hymenoptera venom anaphylaxis.

The plasma concentrations of arginine vasopressin, oxytocin, angiotensin I and II were studied in patients with hymenoptera venom anaphylaxis (n = 50) and healthy volunteers (n = 25). There was no difference in arginine vasopressin: 5.52 +/- 0.45 fmol/ml vs. 3.99 +/- 0.41 fmol/ml or oxytocin: 28.10 +/- 1.13 fmol/ml vs. 26.24 +/- 1.80 fmol/ml between patients and controls. No correlation between the severity of clinical symptoms and the plasma levels of arginine vasopressin and oxytocin was found in patients. However, patients with a history of hymenoptera venom anaphylaxis showed significantly reduced angiotensin I and angiotensin II plasma levels as compared to controls (ANG I: 9.51 +/- 0.61 fmol/ml vs. 22.91 +/- 1.73 fmol/ml; ANG II: 2.84 +/- 0.16 fmol/ml vs. 6.95 +/- 0.33 fmol/ml). A significant inverse correlation between the severity of clinical symptoms and the plasma levels of angiotensin I and angiotensin II was observed; the lower the concentrations the more severe the clinical symptoms. Oxytocin immunoreactivity eluted from the HPLC column as a single peak with the same retention time as synthetic oxytocin. The vasopressin immunoreactive material could be characterized on HPLC as arginine-vasopressin and two other peptides of unknown nature which crossreacted with the vasopressin antibody. These findings suggest a possible role of angiotensin I and angiotensin II in hymenoptera venom anaphylaxis while arginine vasopressin and oxytocin are most likely not involved.

Adolescent↗
PubMed1993

The renin angiotensin system and hymenoptera venom anaphylaxis.

Components of the renin angiotensin system, namely renin, angiotensinogen, angiotensin I and II and aldosterone were measured in plasma of patients with hymenoptera venom anaphylaxis (n = 50) and healthy non-allergic controls (n = 25). Patients with a history of anaphylactic reactions to hymenoptera venom who did not undergo immunotherapy showed significantly reduced renin, angiotensinogen, angiotensin I and angiotensin II in plasma as compared with controls (P < 0.05). There was no difference in the aldosterone concentration between patients and controls. Angiotensin I, angiotensin II, renin and angiotensinogen levels were the same in male and female patients. There was also no difference in the angiotensin I, II, renin or angiotensinogen levels between young and older patients. A significant inverse correlation between the severity of clinical symptoms and the plasma levels of renin (r = -0.382, P < 0.001), angiotensinogen (r = -0.567, P < 0.0001), angiotensin I (r = -0.656, P < 0.0001) and angiotensin II (r = 0.0762, P < 0.0001) was found: the lower the levels the more severe the clinical symptoms. No correlation was found for aldosterone. Hymenoptera venom allergic patients with repeated anaphylactic reactions during hyposensitization did not tolerate the sting of a living insect (n = 6). In these patients, renin, angiotensinogen, angiotensin I and II remained significantly lower than in healthy non-allergic controls. Patients with successful immunotherapy (n = 27) who tolerated the sting of a living insect had renin, angiotensin I and II significantly higher than patients without immunotherapy. These findings suggest a possible role of the renin angiotensin system in hymenoptera venom anaphylaxis.

Adolescent↗
PubMed1993

Measurement and characterization of histamine and methylhistamine in human urine under histamine-rich and histamine-poor diets.

A radioimmunoassay for histamine was used to measure histamine and 1-methylhistamine (MH) in human urine samples. The detection limit of this assay was 2 ng/ml for histamine and 0.5 ng/ml for MH. Cation exchange high performance liquid chromatography (HPLC) on a Bio-Gel TSK SP-5 PW column with gradient elution was capable of separating histamine from its precursor L-histidine and its metabolites MH and 1-methylimidazole acetic acid (MIAA). The concentration of MH-immunoreactive materials in healthy volunteers with no dietary restrictions was 202 +/- 92 micrograms/24 h (mean +/- SD; n = 14). The excretion of MH-like material, expressed as micrograms of MH per 24 h, was not significantly different before or after the intake of histamine-rich food: 217 +/- 88 vs. 276 +/- 135 micrograms/24 h (n = 10). However, in urine samples collected in individual fractions, the levels of MH immunoreactivity were significantly increased after a histamine-rich meal in comparison to the corresponding fractions which were taken a day earlier at the same time intervals after a histamine-low diet (p < 0.03). HPLC characterization of MH immunoreactivity revealed the presence of histamine, MH and a compound with the same retention time as MIAA. The ratio of histamine, MH and MIAA in controls without dietary restrictions, as determined by HPLC analysis, was 50 +/- 6, 47 +/- 5 and 3 +/- 1%, respectively. After a histamine-rich meal the ratio was 97 +/- 2% for histamine, 1% for MH and 2 +/- 1% for MIAA.

Adult↗
PubMed1992

Urinary excretion of angiotensin I, II, arginine vasopressin and oxytocin in patients with anaphylactoid reactions.

Human urine samples, purified on octadecasilyl-silica cartridges, contained immunoreactive angiotensin I, II, arginine vasopressin and oxytocin. The daily excretion of these peptides in healthy volunteers was 190.00 +/- 38.43 (n = 12), 17.48 +/- 3.09 (n = 12), 63.43 +/- 14.84 (n = 8) and 13.52 +/- 1.42 (n = 7) pmol/24 hr, respectively (mean +/- s.e.m.). Patients with a history of anaphylactoid reactions to drugs or food additives showed clinical symptoms such as urticaria, flush, nausea, dizziness and hypotension after oral provocation with cyanocobalamine, propyphenazone, acetylsalicylic acid and sodium benzoate. In five of the seven patients, angiotensin I and II were increased several fold in the urine fractions after symptoms were reported. The average increase in the urine concentration of both peptides was fourfold and 5.5-fold. In three out of five patients, the mean excretion of arginine vasopressin and oxytocin immunoreactive material was also elevated by a factor of 5.7 and 4.4, respectively. Oral provocation with a placebo failed to elicit anaphylactoid symptoms or an increase in the urine levels of angiotensin I or angiotensin II. Angiotensin I and angiotensin II-like immunoreactivity could be characterized on HPLC as Ile5-angiotensin I, Ile5-angiotensin II and angiotensin II metabolites. HPLC characterization of immunoreactive arginine vasopressin and oxytocin in two different gradient systems showed retention times different than the retention times of the corresponding synthetic standard peptides indicating that both peptides are not authentic AVP and OXT. These results suggest that angiotensin I and angiotensin II may be involved in the clinical events observed during some forms of anaphylactoid reactions.

Adult↗
PubMed1992

A naturally occurring opioid peptide from cow's milk, beta-casomorphine-7, is a direct histamine releaser in man.

beta-Casomorphine-7, a naturally occurring product of cow's milk with opiate-like activity, was studied for possible direct histamine liberation activities in humans. It was found to cause concentration-dependent in vitro histamine release from peripheral leukocytes of healthy adult volunteers. Intradermal injection of beta-casomorphine-7 induced a wheal and flare reaction in the skin similar to histamine or codeine. Oral pretreatment with the H1 antagonist terfenadine significantly inhibited the skin responses to beta-casomorphine-7. The intradermal injection of an opiate receptor antagonist, naloxone, inhibited in vitro histamine release and skin reactions only in a 100-fold excess over beta-casomorphine-7. These findings suggest that beta-casomorphine-7 can be regarded as a noncytotoxic, direct histamine releaser in humans. The clinical relevance of these findings deserves further studies.

Adult↗
PubMed1992

Presence of angiotensin peptides in human urine.

Immunoreactive angiotensin I and angiotensin II were found in human urine that was purified on octadecasilylsilica cartridges. The daily excretion of angiotensin I and II in healthy volunteers was 189.00 (SE 38.36) and 17.54 (SE 3.07) pmol/24 h or 148.09 (SE 32.22) and 12.82 (SE 2.34) pmol/L, respectively (n = 12). No circadian rhythm was observed in the excretion patterns of angiotensin I and II. In vitro degradation of angiotensin I or II could not be detected in acidified urine samples. A marked increase in the excretion of angiotensin I and II could be demonstrated in patients with anaphylactoid reactions to drugs and food additives after oral challenge. Immunoreactive angiotensin I and II could be characterized by HPLC as Ile5-angiotensin I, Ile5-angiotensin II, and angiotensin II metabolites.

Adult↗
PubMed1991

In vitro IgE eluation and histamine releasability from peripheral leukocytes of atopics and normals.

The relation between the amount of cell-bound IgE and the histamine 'releasability' of peripheral leukocytes was studied in 28 patients with atopic diseases and 26 non-atopic controls after in vitro stimulation with anti-IgE. Cell-bound IgE was eluted in acid buffer (pH 3.7) and the amount of histamine released (HR) into supernatant at this pH was measured. Incubation with acetate buffer (pH 3.7) induced significantly higher spontaneous HR (32 net percent) in atopics compared to 18% in controls. The amount of IgE eluted was significantly higher in atopics: The calculated number of IgE molecules/basophil was 332,000 in atopics compared to 177,000 in controls. There was a significant positive correlation between plasma IgE and in vitro elutable IgE in atopics (r = 0.73) compared to controls (r = 0.24). After a careful washing procedure attempts were made to 'resensitize' the basophils through incubation with autologous plasma or standard IgE solutions. When resensitization was possible, there was no correlation between histamine releasability after resensitization and original IgE content of basophils. It is concluded that the increased histamine releasability from leukocytes of atopic individuals after stimulation with anti-IgE is only in part due to an increased number of IgE molecules per basophil surface. A non-specific increased releasability was demonstrated by increased spontaneous HR rates in acid buffer (pH 3.7). A resensitization with autologous plasma-IgE was possible only in half of the subjects investigated, most of them being atopic. The data support the concept of an altered releasability both towards IgE-dependent and independent stimuli being one possible factor in the pathogenesis of atopic eczema.

Adolescent↗
PubMed1990

High-performance liquid chromatography for the separation of angiotensin and its metabolites in human plasma and sweat.

A reversed-phase high-performance liquid chromatography (HPLC) method with gradient elution for the separation of angiotensin peptides is described. The highly reproducible method allows the base-line separation of angiotensin peptides with UV detection at 225 nm. This chromatographic methodology in combination with radioimmunoassay (RIA) is used for the characterization of angiotensin peptides in human plasma and sweat.

Acetonitriles↗
PubMed1989

Chromatographic methods for characterization of angiotensin in brain tissue.

Ang II antiserum with high sensitivity and specificity was produced. The native Ang II antiserum was purified by affinity chromatography on Affi-Gel 102 with covalently coupled [Ile5]Ang II, and purified Ang II antiserum was covalently coupled to Affi-Gel 10. The column with the covalently coupled Ang II antiserum was used for the specific enrichment of Ang II from brain extracts. The efficiency and usefulness of affinity chromatography for the purification of Ang II from biological sources were tested with 125I-labeled, 3H-labeled, and synthetic [Ile5]Ang II added to rat brains prior to extraction. In addition, the methodology was used for the purification of endogenous Ang II from pig brain. The described three-step procedure for the isolation and purification of Ang II including extraction, affinity chromatography, and HPLC is rapid and highly specific with high loading capacity. We have applied the method to the peptide Ang II in brain, but the methodology may also be used in general for the rapid purification of other neuropeptides. A combination of HPLC with specific radioimmunoassays for Ang I and Ang II was utilized to demonstrate that rat brain cells in culture devoid of the influence of the peripheral RAS were able to synthesize radioactively labeled Ang I and Ang II after incubation with [3H]isoleucine. And, finally, an HPLC system capable of separating Ang I, Ang II, and its metabolites was used to obtain insight into the degradation pattern of angiotensin peptides in the brain. Aminopeptidases appear to be the major angiotensin-degrading enzymes, and endopeptidases do not appear to be involved.

Angiotensin II↗
PubMed1989

Metabolism of angiotensin peptides by neuronal and glial cultures from rat brain.

The degradation pattern and rate of [Ile5]-Angiotensin (Ang) I, II, and III were studied in neuron-enriched and glia-enriched cells in primary cultures from rat brain. Metabolites were separated by HPLC, and their identities were evaluated by comparison of their retention times with those of synthetic Ang peptide fragments and by analysis of their amino acid composition. Major metabolites were identified as des-Asp1-[Ile5]-Ang I, des-Asp1-[Ile5]-Ang II, [Ile5]-Ang II (3-8) hexapeptide, [Ile5]-Ang II (4-8) pentapeptide, and [Ile5]-Ang II (5-8) tetrapeptide. Glia-enriched cells degraded [Ile5]-Ang I and [Ile5]-Ang III significantly faster than neuron-enriched cells, whereas no difference between the two types of cells was found in the degradation rate of [Ile5]-Ang II. Although the half-lives of [Ile5]-Ang I and [Ile5]-Ang III in neuron-enriched cells from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were not significantly different, neuron-enriched cultures from WKY rats metabolized [Ile5]-Ang II about 2.6 times faster than neuron-enriched cells derived from SHR.

Angiotensin I↗
PubMed1989

Release of immunoreactive angiotensin II from neuronal cultures: adrenergic influences.

The effects of adrenergic drugs on the release of immunoreactive angiotensin II (ANG II-ir) from brain cells in culture were examined. In neuronal cultures, basal release of Ang II-ir was 43.65 +/- 7.44 pg/5-min incubation period (n = 14 experiments; 52 individual determinations), and in astrocytic glial cultures, it was 21.76 +/- 5.7 pg (n = 8 experiments; 24 individual determinations) when cells were exposed to buffer alone. Incubation of neuronal cultures with the alpha 2-adrenergic antagonist yohimbine (0.1-50 microM, 5 min) caused concentration-dependent increases in ANG II-ir release above basal levels. Analysis of the released material by high-pressure liquid chromatography revealed that authentic ANG II was present. No increase in the release of ANG II-ir was seen from glial cells. Experiments using neuronal cultures revealed that the yohimbine-induced release of ANG II-ir may be secondary to increased norepinephrine (NE) release. Incubation of neuronal cultures with NE (10 nM-50 microM) caused concentration-dependent increases in the release of ANG II-ir. This effect of NE was not inhibited by the alpha 1-adrenergic blocker prazosin. However, a weaker release of ANG II-ir from neuronal cultures was stimulated by the beta-adrenergic agonist isoproterenol at 100 microM. These data show that ANG II-ir can be released from neuronal but not glial cell cultures by adrenergic receptor-mediated mechanisms.

Adrenergic alpha-Agonists↗
PubMed1988

Biosynthesis of angiotensinogen and angiotensins by brain cells in primary culture.

This study focuses on the ability of primary rat brain cells in culture to synthesize angiotensinogen, angiotensin I, and angiotensin II. HPLC in combination with radioimmunoassay was used to characterize these compounds. Following incubation with 3H-labeled isoleucine, radioactively labeled angiotensinogen with an approximate molecular weight of 25,000 was identified in both glial and neuronal cells. Other molecular weight forms of angiotensinogen with molecular weights of about 300 and 160,000 were present in both cell types. In addition to angiotensinogen, radioactively labeled angiotensin I and angiotensin II were also synthesized by neuronal and glial cells. These results suggest that glial and neuronal cells can synthesize angiotensinogen, angiotensin I, and angiotensin II in a similar manner shown for the peripheral renin angiotensin system.

Angiotensin I↗
PubMed1988

Immunocytochemical and biochemical characterization of angiotensin I and II in cultured neuronal and glial cells from rat brain.

Neuronal and glial cells cultured from neonatal rat brains showed staining for both angiotensin I and II using the peroxidase-antiperoxidase method. In glial cell extracts of normotensive Wistar-Kyoto rats, the concentrations of angiotensin I and II were 12.47 +/- 2.71 (n = 4) and 66.73 +/- 13.28 fmol/mg protein (n = 4). Angiotensin I and II found in neuronal cell extracts of normotensive Wistar-Kyoto rats were 11.29 +/- 2.99 (n = 4) and 60.25 +/- 12.77 fmol/mg protein (n = 4). No significant difference was found in the concentration of angiotensin I and II in both cell types from the same rat strain. Angiotensin I concentrations of 16.83 +/- 3.43 fmol/mg protein (n = 5) determined in neuronal cell extracts derived from spontaneously hypertensive rats did not differ significantly from those found in neuronal cell extracts of Wistar-Kyoto rats. However, neuronal cell extracts from spontaneously hypertensive rats revealed values of 25.19 +/- 4.31 fmol angiotensin II/mg protein (n = 4). This was significantly different (p less than 0.05) and represented a 58% reduction in the angiotensin II levels in neuronal cells from spontaneously hypertensive rats compared to Wistar-Kyoto rat cultures. Angiotensin I and II measured in the growth medium containing 10% plasma-derived horse serum was below the detection limit of both radioimmunoassays. No difference in the angiotensin I and II levels was found in cells kept in serum-free medium. The angiotensin I and II immunoreactive material determined in the cell extracts could be characterized on reversed-phase high pressure liquid chromatography as (Ile5)-angiotensin I and II. (Ile5)-angiotensin III was not detectable.

Angiotensin I↗
PubMed1988

Measurement and characterization of angiotensin peptides in plasma.

We report a method for the extraction of angiotensin peptides from plasma with a mixture of acetone, 1 mol/L HCl, and water (40/1/5 by vol). The method is highly reproducible for the measurement of angiotensin I and angiotensin II in small sample volumes, with analytical recoveries of about 80% for both peptides. We investigated the influence of sample handling and found a standard procedure for blood collection, plasma preparation, and extraction was essential. The method was used to measure angiotensin I and II in rat and human plasma. In rat plasma, the mean (+/- SEM) concentrations of angiotensin I and angiotensin II were determined to be 67 (+/- 8) and 14 (+/- 1) pmol/L (n = 10), respectively. Neither angiotensin I nor angiotensin II was detectable 24 h after bilateral nephrectomy. Acute oral administration of the converting-enzyme inhibitor ramipril caused a significant increase of angiotensin I from 85 (+/- 6) to 257 (+/- 33) pmol/L (n = 10; P less than 0.001) and a significant decrease of angiotensin II from 12 (+/- 1) to 7 (+/- 0.4) pmol/L in rat plasma (n = 9; P less than 0.001). In human plasma, angiotensin I and angiotensin II values of 21 (+/- 1) and 6.6 (+/- 0.5) pmol/L (n = 10) were found. A single oral dose of the diuretic furosemide increased angiotensin I significantly from 21 (+/- 1) to 32 (+/- 1.7) pmol/L (n = 5); P less than 0.001), whereas angiotensin II remained unchanged, 6.6 (+/- 0.5) vs 6.4 (+/- 0.4) pmol/L (n = 5). Extracted peptides could be identified as [IIe5]-angiotensin I and [IIe5]-angiotensin II by HPLC in combination with specific radioimmunoassays for angiotensin I and angiotensin II.

Adult↗