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Biomedical subjects

U Walter

Publications and source records attributed to U Walter.

At least 217 records · Page 12Linked to original sources
PubMed1978

Adenosine 3':5'-monophosphate receptor proteins in mammalian brain.

cAMP receptor proteins present in mammalian brain were identified and characterized with the use of the photoaffinity label 8-azido[32P]cAMP. Cytosol and membrane fractions from various regions of rat, guinea pig, and bovine brain contained two specific cAMP receptor proteins with apparent molecular weights of 47,000 and 52,000 to 55,000. Subcellular fractionation studies showed the highest amounts of these cAMP receptor proteins associated with cytosol fractions and synaptic membrane fractions. For both the cytosol and membrane fractions, the two cAMP receptor proteins represented almost all of the proteins specifically labeled by 8-azidol[32P]cAMP and appeared to be the regulatory subunits of cAMP-dependent protein kinases.

Affinity Labels↗
PubMed1978

Quantitative labeling of the regulatory subunit of type II cAMP-dependent protein kinase from bovine heart by a photoaffinity analog.

Several methods were compared for estimating the amount of regulatory subunit of an 800-fold purified Type II cAMP-dependent protein kinase from bovine heart. These methods included a reversable binding assay using either cAMP, or 8-N3-[32P]cAMP, photoaffinity labeling with 8-N3-[32P]cAMP, and autophosphorylation of the regulatory subunit of the enzyme. Although the regulatory subunit had a slightly lower affinity for 8-N3-cAMP than for cAMP, the total amount of regulatory subunit could be determined by each of the procedures examined. The results indicate that the photoaffinity analog 8-N3-[32P]cAMP is able to label quantitatively all cAMP-binding sites of the regulatory subunit of this cAMP-dependent protein kinase.

Affinity Labels↗
PubMed1978

Protein kinases in developing rat brain.

The levels of cAMP-dependent protein kinases were measured in developing rat brain by a variety of methods. The regulatory subunit (R) was measured both by [3H]cAMP binding and by 8-N3-[32P]cAMP incorporation. The catalytic subunit (C) was measured by an assay of histone kinase activity. Data were calculated per mg protein. Neither R nor C levels changed significantly in either membranes or cytosol during development. The ratio of R to C was essentially unity in the cerebra of both newborn (2-day-old) and adult (40-day-old) rats. Polyacrylamide-gel electrophoresis resolved two regulatory subunits (R-I) and (R-II) which were derived from the Type I and Type II cAMP-dependent protein kinases, respectively. 8-N3-[32P]cAMP incorporation into Proteins R-I and R-II indicated that the amounts of Proteins R-I and R-II did not change significantly in either membranes or cytosol during development.

Aging↗
PubMed1977

Study of autophosphorylation of isoenzymes of cyclic AMP-dependent protein kinases.

Type I and type II cyclic AMP-dependent protein kinases, present in the cytosol from each of five rat and two bovine tissues, were separated from one another by DEAE-cellulose column chromatography in order to study their possible autophosphorylation. In each of the tissues studied, autophosphorylation of the regulatory subunit of the cyclic AMP-dependent protein kinase by the catalytic subunit could be demonstrated with the type II enzyme but not with the type I enzyme.

Animals↗
PubMed1977

Identification, characterization, and quantitative measurement of cyclic AMP receptor proteins in cytosol of various tissues using a photoaffinity ligand.

Two protein bands, present in cytosol fractions from each of seven rat tissues examined, specifically incorporated 32P-labeled 8-azidoadenosine 3':5'-monophosphate (8-N3-[32P]cAMP), a photoaffinity label for cAMP-binding sites. These proteins had apparent molecular weights of 47,000 and 54,000 on a sodium dodecyl sulfate-polyacrylamide gel electrophoresis system. These two proteins were characterized in three of the tissues, namely, heart, uterus, and liver, by the total amount of 8-N3-[32P]cAMP incorporation, by the dissociation constant (Kd) for 8-N3-[32P]cAMP, and by the nucleotide specific inhibition of 8-N3-[32P]cAMP incorporation. Several lines of evidence were obtained that the protein with an apparent molecular weight of 47,000 represents the regulatory subunit of a type I cAMP-dependent protein kinase, while the protein with an apparent molecular weight of 54,000 represents the regulatory subunit of a type II cAMP-dependent protein kinase. Almost all of the cAMP receptor protein found in the cytosol of these tissues, as measured by 8-N3-[32P]cAMP incorporation, was associated with these two protein kinases, in agreement with the idea that most effects of cAMP are mediated through protein kinases. The photoaffinity labeling with 8-N3-[32P]cAMP can be used to estimate quantitatively the amounts of regulatory subunit of type I and type II cAMP-dependent protein kinases in various tissues.

Affinity Labels↗
PubMed1977

Low renin hypertension.

Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.

Adrenal Cortex↗
PubMed1976

[Studies on the pH-dependence, inhibition and reactivation of angiotension II-amide splitting enzymes in human erythrocytes (author's transl)].

Aminopeptidase activity of three fractions of human erythrocytes (membranes free of hemoglobin; hemolysate free of membranes; enzyme protein fraction made free of hemoglobin by DEAE-cellulose) was measured by a NADH dependent optical test using asparaginyl1-angiotension II-amide as substrate. 1. From the enzyme protein fraction 6 subfractions were obtained by (NH4)2SO4 precipitation. By measuring enzyme kinetics at three different pH-values (pH 5,0; 7,0; 8,0) with and without addition of the effectors Na2EDTA and Ca++ the existence of 6 different enzymes could be demonstrated. 2. The aminopeptidase activity of the hemolysate made free of membranes could be inhibited by diisopropylfluorphosphate and p-chloromercuribenzoate at three different pH-values (pH 5,0; 6,5; 7,0; 8,0 and 6,5; 7,0; 8,0 respectively). 3. A reduction of enzymatic activity of 20% was found after incubation at 37degreesC for two hours.

Calcium↗
PubMed1976

[Diurnal profiles of plasma aldosterone, cortisol, renin, angiotensinogen and angiotensinases in normal subjects (author's transl)].

Plasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20-26) under control conditions and subsequently under suppression of ACTH release by dexamethasone. Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations. Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period. Similar to aldosterone, renen showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone. No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.

Adrenocorticotropic Hormone↗