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Biomedical subjects

R Kreutz

Publications and source records attributed to R Kreutz.

At least 73 records · Page 4Linked to original sources
PubMed1994

Differential regulation of vascular angiotensin I-converting enzyme in hypertension.

The angiotensin I-converting enzyme (ACE) gene is found on the locus that has been linked to high blood pressure after sodium loading in rats, so in the present study we investigated the role of vascular ACE for the pathophysiology of hypertension in the corresponding parental strains, Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP), in basal conditions at different ages and after sodium loading. Blood pressure was already significantly enhanced in SHRSP from 4 weeks of age, and sodium loading induced an additional increase only in the hypertensive strain. In the aorta, basal ACE gene expression, analyzed by quantitative polymerase chain reaction, and ACE activity were similar in both strains, whereas mRNA levels were elevated in SHRSP after salt compared with WKY rats and correlated with an increase in enzymatic activity. In mesenteric arteries, ACE mRNA levels were significantly enhanced in SHRSP at all ages, although ACE activity was not different between the strains. These results were not modified after sodium loading. These data demonstrate that the level of ACE activity in plasma and vascular tissue can be controlled in a different manner within a rat strain and that in contrast to the soluble form, the membrane-bound ACE may be the one responsible for determining the vasoactive effects of angiotensin II. In addition, ACE undergoes a different regulation in vascular tissues of SHRSP compared with WKY rats, which might be involved in the regulation of blood pressure in these animals.

Aging↗
PubMed1994

Augmented agonist-induced Ca(2+)-sensitization of coronary artery contraction in genetically hypertensive rats. Evidence for altered signal transduction in the coronary smooth muscle cells.

The Ca2+ responsiveness of vascular smooth muscle myofilaments is not unique: it is increased during neuro-humoral activation and decreased during beta-adrenergic stimulation. In this study we tested whether an augmented Ca2+ responsiveness of smooth muscle myofilaments may contribute to the increased coronary tone observed in hypertension using beta-escin-permeabilized coronary arteries from 3-mo-old stroke-prone spontaneously hypertensive rats (SHRSP) and their age matched normotensive reference strain (WKY rats). In intact coronary arteries, the response to 5-hydroxytryptamine (5-HT) but not to KCl was larger in SHRSP than in WKY rats. In beta-escin permeabilized coronary arteries in which the receptor effector coupling is still intact, 5-HT enhanced force at constant submaximal (Ca2+) (pCa 6.38) to a greater extent in SHRSP. The Ca2+ sensitizing effect of 5-HT was mimicked by GTP gamma S (0.01-10 microM); again this effect was larger in SHRSP. In the absence of 5-HT or GTP gamma S the Ca2+ force relation was similar in both groups. Forskolin induced relaxation at constant submaximal (Ca2+). This desensitizing effect was smaller in SHRSP than in WKY rats. In conclusion, this study shows that intracellular signalling pathways involved in modulating the Ca2+ responsiveness of coronary smooth muscle myofilaments are altered in the genetically hypertensive animals favoring a hypercontractile state in the coronary circulation.

Actin Cytoskeleton↗
PubMed1993

[Primary hyperreninemia. An unusual cause of secondary arterial hypertension].

In 1975, scintigraphy revealed a 6.5 x 5 cm tumour in the region of the left adrenal in a 36-year-old man with known hypertension for 5 years (systolic pressure up to 250 mm Hg, diastolic up to 130 mm Hg). A laparotomy was performed for a suspected phaeochromocytoma. A tumour was located in the upper pole of the kidney and removed together with the kidney. The blood pressure quickly returned to normal after the operation: it remained stable for the following 17 years (between 130/80 to 150/90 mm Hg). Originally the tumour could not be clearly classified either clinically or histologically. But recently the paraffin-imbedded tumour specimen was re-examined by immunohistochemistry and in-situ hybridization. This identified a renin-producing tumour so that primary reninism was the cause of the arterial hypertension.

Adult↗
PubMed1993

Membrane microviscosity does not correlate with blood pressure: a cosegregation study.

OBJECTIVE: To determine whether elevated microviscosity is associated with elevated arterial pressure in segregating (F2) hybrids produced by crossing stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats. METHODS: SHRSP and WKY rats were obtained from the colony at the University of Heidelberg. F2 progeny were obtained by brother-sister mating of the F1 progeny of the cross between SHRSP and WKY rats. Membrane microviscosity (the inverse of fluidity) was measured as a fluorescence anisotropy of trimethylammonium diphenylhexatriene incubated with the erythrocyte membranes. The measurements were made using a luminescence spectrometer with computer-controlled excitation and emission polarizers. RESULTS: Membrane microviscosity was significantly greater (fluidity was lower) in erythrocyte membranes obtained from SHRSP than in those obtained from WKY rats. In the F2 cohort there were no significant correlations between membrane microviscosity and systolic blood pressure, diastolic blood pressure, salt-loaded systolic blood pressure or salt-loaded diastolic blood pressure. A similar lack of relationship between these parameters was shown in a subgroup analysis, in which males or females with a male WKY rat progenitor and males or females with a male SHRSP progenitor were analysed separately. CONCLUSIONS: Erythrocyte membrane microviscosity is elevated in SHRSP compared with WKY rats. In segregating F2 hybrid rats the membrane microviscosity trait does not correlate with blood pressure. These results eliminate the microviscosity trait as being directly related to the cause of genetic differences in blood pressure between WKY rats and SHRSP.

Animals↗
PubMed1993

Ontogenetic regulation of mouse Ren-2d renin gene in transgenic hypertensive rats, TGR(mREN2)27.

TGR(mREN2)27 is a new monogenetic rat model with fulminant hypertension, low kidney renin, and high extrarenal renin gene expression. This study characterizes and compares expression of the Ren-2 gene in TGR(mREN2)27 with that in DBA/2 mice and with renin gene expression in rats. Except in the submandibular gland, the tissue-specific expression of Ren-2 is similar in TGR(mREN2)27 and DBA/2. This demonstrates maintenance of tissue specificity. Organs that are involved in cardiovascular regulation, such as the adrenal gland, kidney, and brain, express the Ren-2 gene before hypertension has developed, consistent with the possibility of a causal relationship between transgene expression in these tissues and hypertension. Because these tissues express the renin gene in nontransgenic rats as well, we suggest that this model can be used to study the regulation of renin gene expression and its role in hypertension at these sites. In addition, as an indication that interactions may exist between blood pressure and renin gene expression, we describe reciprocal changes in blood pressure and Ren-2 mRNA levels in the kidney and brain.

Adrenal Glands↗
PubMed1992

Analysis of the envelope region of the highly divergent HIV-2ALT isolate extends the known range of variability within the primate immunodeficiency viruses.

HIV-2ALT is a highly divergent HIV-2-related isolate that is genetically equidistant to the prototypic HIV-2 strains, defined by HIV-2ROD, and to the simian immunodeficiency viruses SIVmac and SIVsm. We have now cloned and sequenced the envelope region of HIV-2ALT, thus completing the analysis of the whole viral genome. The sequences of env and nef and of the second exons of tat and rev were compared with those of the other viruses of the HIV-2/SIVsm/SIVmac group. Despite of the high degree of variation of HIV-2ALT, functional domains of the genes are conserved. Although in env, the overall pattern of constant and variable domains is maintained, many single amino acid exchanges exist at positions previously thought to be constant in HIV-2 strains. In addition, when compared with a broader spectrum of immunodeficiency viruses, which includes SIVMND from mandrill and SIVAGM from African green monkey, HIV-2ALT Env has a high percentage of amino acid exchanges, which are unique to this strain. This underlines the separate branch of HIV-2ALT within the phylogenetic tree and makes obvious the inclusion of such divergent strains in preventive and therapeutic programs.

Amino Acid Sequence↗
PubMed1992

Molecular genetics of hypertension.

During the last decades the evidence that a genetic component contributes to the development of primary hypertension has been accumulating. The identification of the genes involved in blood pressure regulation, however, is only starting to emerge. The recent advances in recombinant DNA technology provide new molecular genetic strategies in cardiovascular research. In this review we will discuss the testing of candidate genes in vivo by transgenic techniques. Furthermore, we will describe the possibilities to identify the genes implicated in primary hypertension by genetic linkage analysis using polymorphic DNA markers.

Animals↗
PubMed1989

Molecular cloning of two west African human immunodeficiency virus type 2 isolates that replicate well in macrophages: a Gambian isolate, from a patient with neurologic acquired immunodeficiency syndrome, and a highly divergent Ghanian isolate.

Human immunodeficiency virus type 2 (HIV-2)-related viruses were isolated from a Gambian dying of exclusively neurological disease (HIV-2D194) and from an asymptomatic Ghanian (HIV-2D205). Both strains exhibited properties of HIV-1 biological subtype c: they grew slowly and induced few or no syncytia but eventually produced high levels of particle-associated reverse transcriptase in cultures of fresh peripheral blood lymphocytes, and they established stable infection of T-lymphoma (HUT-78) and monocytic (U937) cell lines. Each produced even higher levels of reverse transcriptase when fresh human monocytes/macrophages were used as target cells. The viruses were molecularly cloned after a single passage in culture, in order to minimize in vitro selection of subtypes present in vivo. Restriction-site analysis showed heterogeneity within each isolate. Nucleotide sequence analysis of a portion of the HIV-2D194 genome revealed that it is a member of the prototypic HIV-2 family, displaying 13% divergence versus HIV-2ROD and HIV-2NIHZ, as compared to 9% divergence between HIV-2ROD and HIV-2NIHZ. In contrast, HIV-2D205 is the most highly divergent HIV-2 strain yet described: it is equidistant in relation between the known HIV-2 strains and the simian immunodeficiency virus isolates from rhesus macaque monkeys (23-25% divergence).

Acquired Immunodeficiency Syndrome↗
PubMed1981

[Cartilage channels of the human patella up to birth].

In the human patella from the 4th month up to the birth were examined contents and surrounding structures of vascular channels. Except the articular area the cartilage of the patella is covered by the perichondrium. From here mesenchym and blood vessels enter, and penetrate into the cartilage by forming channels. Dependent on the stages of development the construction of cartilage around the channels is different in comparison with other territories. The findings will be compared with the results from the channels in the cartilaginous anlage of different bones.

Cartilage↗
PubMed1981

[Investigation on the influence of trimethoprim at the intrauterine development in the rat (author's transl)].

The present investigations was made to check the effects of repeated oral applications of the chemotherapeutic effective pirimidinsubstance trimethoprim (pure substance) at the intrauterine development in the wistar rat. The agent was given with a throat tube suspended in hydroxyacetylcellulose from the 5th to the 7th, from the 8th to the 10th and from the 11th to the 13th day p. c. The dosage was 1,500, 1,000, 750 and 200 mg trimethoprim per kg bodyweight. The valuation of the fetal development was made after the subsequent parameters: mean implantationrate, resorptionrate, mean fetal bodyweight. Statement of anomalies by inspection of the body surface shape and the brightened skeleton. The dosage of 200 mg TMP/kg bodyweight influences the fetal development only a little. Doses of 1,500, 1,000, and 750 mg TMP/kg bodyweight however show a high toxicity for the used rat strain as well for the mother animals as for the fetuses of the surviving animals. The observed increased resorption rates diminishing of the average fetal bodyweight, anomalies of the body shape and different anomalies of the skeleton are typical effects of folic acid antagonists.

Abnormalities, Drug-Induced↗
PubMed1979

[The effect of repeated applications of carbutamide on the embryonic development of the rat (author's transl)].

The present paper will check the effects of repeated applications of the oral "antidiabeticum" Carbutamide (substitute of the "sulfonylurea") on the embryonic development of wistar rats. The agent was given the pregnant animal by the means of a throat sonde at the 5th, 6th and 7th day post coitum suspended in Tween 80 in a dosage of 800 mg/kg bodyweight. In order to value the intrauterine development the following parameters were used: mean implantation rate, resorptions rate, bodyweight of fetuses, statemend of animalies by an accurate inspection of the body surface shape, of the skeleton and the inner organs. The rates of implantation do not differ from that of the control group. The rate of resorption increases dependend on the beginning of the treatment. The later the treatment begins the higher the resorptions rate. The body weight of surviving fetuses is diminished strongly. Damage of the skeleton appears as the presence of 14th ribs at one or each side or as ossifications at the 7th neck vertebra (neck rib). Also this results depend on the beginn of the treatment.

Abnormalities, Drug-Induced↗