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Biomedical subjects

K Hermann

Publications and source records attributed to K Hermann.

At least 91 records · Page 5Linked to original sources
PubMed1983

The tissue renin-angiotensin systems: focus on brain angiotensin, adrenal gland and arterial wall.

The enzyme renin has long been considered an exclusively renal enzyme responsible for the generation of angiotensin in the plasma, and angiotensin was considered a peptide hormone with specific target organs. Since renin has been discovered to occur not only in the kidney but in addition in a large number of other tissues, e.g. the salivary gland, the uterus, the blood vessels, the adrenal gland and the brain, this concept had to be revised. The possibility of local generation of angiotensin in these target tissues, where it has marked biological effects casts a new light on angiotensin as a more ubiquitous tissue factor or even a neurohormone.

Adrenal Glands↗
PubMed1983

The brain angiotensin system: subcellular localization and interferences with converting enzyme inhibitors.

Renin is stored in synaptosomes of rat brain, separately from cathepsin D and intraneuronal angiotensin II (ANG II) has been demonstrated with the electron-microscope. Although the subcellular localization of other components of the renin-angiotensin system (RAS) have still to be investigated, these data suggest possible intracellular synthesis of ANG II in the brain. Brain ANG II is biochemically identical to the plasma peptide and corresponds to (IIe) 5-ANG II. The peptide level is unchanged after bilateral nephrectomy, and angiotensin I (ANG I) accumulation is observed in nephrectomized animals following brain angiotensin converting enzyme blockade. The significantly greater accumulation of ANG I and reduction of ANG II in stroke prone spontaneously hypertensive Wistar-Kyoto rats (WKY) indicates a higher synthesis and turnover rate of ANG II in SHR. Most converting enzyme inhibitors (CEI) penetrate the brain after chronic oral treatment. Part of their blood pressure lowering action may therefore be explained by an inhibition of the brain RAS.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Distribution of neurophysins in rat brain: radioimmunological measurement and characterization.

Rat neurophysins were isolated from posterior pituitaries and antibodies raised in rabbits. Individual sensitive and specific radioimmunoassays for the neurophysins associated with either vasopressin or oxytocin were developed and employed for measuring the neurophysins in various regions of rat brain. Neurophysin-like immunoreactivity was detected in hypothalamus, septum, amygdala, brainstem and spinal cord. Characterization by high performance liquid chromatography suggested the identity with the neurophysins contained in the posterior pituitary. The distribution of these peptides in the brain points to a possible role in central nervous system processes.

Animals↗
PubMed1982

Kininogenase activity in rat uterus homogenates.

A synthetic peptide substrate for tissue kallikreins was hydrolysed by uterus homogenates. These also released kinins when incubated with dog kininogen. By using high pressure liquid chromatography in combination with a radioimmunoassay for kinins, the peptides released were identified as bradykinin and kallidin. Plasma kallikrein and trypsin released bradykinin from dog kininogen and hog pancreas kallikrein released kallidin from this substrate. This suggests that a tissue kallikrein and also a trypsin-like enzyme or perhaps plasma kallikrein are present in rat uterus.

Animals↗
PubMed1967

Thyroid disease following the administration of thorotrast.

Four cases of thyrotoxicosis are reported among 35 patients who had been given Thorotrast during the investigation of intracranial haemorrhage. For the group as a whole Thorotrast had been given between 11 and 31 years (mean 23.4 years) before this study. Thyrotoxicosis occurred in four patients between six and 17 years (mean 11.8 years) after the injection of Thorotrast. The fact that thyrotoxicosis did not occur in a small control group of patients who had had a subarachnoid haemorrhage and in whom Thorotrast had not been used at angiography suggests that Thorotrast may be of aetiological significance. In view of the known association between thyrotoxicosis and changes in the lymphoreticular system it is possible that the irradiation of this system by retained thorium has resulted in an abnormality of function which renders these patients more liable to the development of thyrotoxicosis.A fifth patient developed non-toxic thyroid enlargement 16 years after Thorotrast angiography.

Adult↗
PubMedDate not supplied

Antihypertensive action of the converting enzyme inhibitor perindopril (S9490-3) in spontaneously hypertensive rats: comparison with enalapril (MK421) and ramipril (Hoe498).

The novel prodrug-converting-enzyme (CE) inhibitor perindopril (S9490-3) diacid was found to be as potent as ramipril (Hoe498) diacid and more potent than enalapril (MK421) diacid and captopril against rat plasma CE in vitro (IC50 values were 3 X 10(-9), 2 X 10(-9), 1 X 10(-8), and 6 X 10(-8) mol/L, respectively). Four-week oral treatment with perindopril (0.1, 1, 3, and 10 mg/kg/day) in spontaneously hypertensive rats (SHRSP) lowered blood pressure (BP) dose-dependently with a threshold dose of 0.1 mg/kg/day and normalization of BP following doses between 1-3 mg/kg/day. Plasma CE was inhibited, angiogensinogen lowered, plasma renin concentration (PRC) and angiotensin I (ANGI) increased, all dose-dependently. CE was also inhibited in kidney, aortic wall, heart, lung, hypophysis, and brain cortex. Upon drug withdrawal, the BP depressant effect outlasted the effects on the plasma renin-angiotensin system (RAS) by more than a week. Perindopril, ramipril (both 1 mg/kg/day), and enalapril (30 mg/kg/day) showed equal antihypertensive actions in SHRSP, although their effects on parameters of the RAS in plasma were different. Our data reveal perindopril to be a potent antihypertensive drug. The findings are consistent with the view that the antihypertensive actions of CE inhibitors cannot be directly related to inhibition of the RAS in the plasma. Local interference with the RAS in tissue appears to be an additional factor involved.

Administration, Oral↗
PubMedDate not supplied

Mismatch repair deficiency in sporadic synchronous colorectal cancer.

BACKGROUND: Hereditary non-polyposis colorectal cancer (HNPCC) patients frequently develop synchronous colorectal cancer (SCRC) which also occurs sporadically in other patients. Recent studies on microsatellite instability (MSI) in sporadic SCRC diverge completely in their findings (0%-100%). In the present study MSI and mismatch repair (MMR) proteins were evaluated according to standardised criteria (exclusion of a family history, MSI analysed according to NCI recommendations) METHODS: Paraffin embedded sections of SCRC of 30 patients were evaluated for MSI and the loss of protein expression of hMLH1 and hMSH2. RESULTS: 3 out of 30 (10%) patients exhibited MSI-H which 5 out of 30 (17%) showed MSI-L. Loss of protein expression of either hMLH1 or hMSH2 was found in all cases of MSI-H and none of the MSI-L cancers. CONCLUSION: MSI is found in sporadic cases of SCRC to about the same extent as it is mentioned in the literature on sporadic single colorectal cancers. Immunohistochemistry with mismatch repair proteins could be used as a pre-screening for MMR deficiency in sporadic SCRC.

Adaptor Proteins, Signal Transducing↗