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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 721 records · Page 40Linked to original sources
PubMed1985

Presence of a 1,25-dihydroxy-vitamin D3 receptor in chick skeletal muscle myoblasts.

The presence of a specific receptor for 1,25-dihydroxy-vitamin D3 was investigated in myoblasts released from chick embryo skeletal muscle by trypsin and collagenase treatment. Density gradient analysis of the cytosol obtained from these muscle cell preparations showed that 1,25-dihydroxy-vitamin D3 binds specifically to a 3.7 S macromolecule. Scatchard analysis yielded an equilibrium dissociation constant of 2.46 x 10(-10) M and a Nmax of 74 fmol/mg of cytosol protein. The data is in agreement with previous evidence which indicates that the action of the vitamin D metabolite on muscle Ca uptake is mediated by de novo protein and RNA synthesis, and supports the concept that muscle is a target organ for 1,25-dihydroxy-vitamin D3.

Animals↗
PubMed1985

Nuclear testicular 1,25-dihydroxyvitamin D3 receptors in Sertoli cells and seminiferous tubules of adult rodents.

1,25(OH)2D3 receptors were studied in whole testes, Sertoli cells, seminiferous tubules, Leydig cells and spermatogonia of adult NMRI mice and SD rats. Specific reversible high affinity binding (KD 1.4 x 10(-10)M; Nmax 72 fmol/mg protein) by a 3.5 S macromolecule was demonstrated in whole testes, Sertoli cells and seminiferous tubules. With identical techniques, no receptors were found in Leydig cells despite previous reports of 1,25(OH)2D3 actions on Leydig cell function.

Animals↗
PubMed1985

Blood pressure and metabolic control as risk factors for nephropathy in type 1 (insulin-dependent) diabetes.

The respective rôles of arterial blood pressure and metabolic control in different stages of diabetic nephropathy were analyzed retrospectively in 52 sequentially-followed Type 1 (insulin-dependent) diabetic patients. A negative correlation was found between median post-prandial blood glucose and median duration of diabetes until onset of persistent proteinuria (p less than 0.01). Systolic blood pressure was higher in patients who subsequently developed persistent proteinuria than those who did not (140 versus 121 mmHg; p less than 0.05), but duration of the interval until onset of persistent proteinuria was not related to blood pressure. After onset of persistent proteinuria, hypertensive diabetic patients developed elevated serum creatinine concentrations more frequently than normotensive diabetic patients (67% versus 14%, p less than 0.05). In these patients, the delay until elevation of serum creatinine concentration was negatively correlated with blood glucose (p less than 0.01). Once serum creatinine was raised, decay of renal function occurred faster in patients with persistent than intermittent hypertension (p less than 0.05). No effect of metabolic control was demonstrable at this stage of nephropathy. It is concluded that metabolic control determines the early course of diabetic nephropathy, whereas blood pressure is more important in advanced stages of nephropathy.

Adolescent↗
PubMed1985

Abnormal radiofurosemide binding by Tamm Horsfall glycoprotein of diabetic patients.

In the present study, 8 Type 1 diabetic patients with normal creatinine clearance and 8 matched controls were examined. Tamm Horsfall glycoprotein was isolated with the NaCl precipitation procedure. Its purity was checked by gel-electrophoresis, immunodiffusion and isoelectric focussing. Tamm Horsfall glycoprotein of diabetic patients had higher glucose (p less than 0.05) and lower N-acetylneuraminic acid content (p less than 0.01) than controls. 14C-furosemide binding by Tamm Horsfall glycoprotein was examined using an Amicon ultrafiltration system at 0 degree C. In nominally sodium-free medium, furosemide binding by Tamm Horsfall glycoprotein was significantly (p less than 0.01) higher in diabetic patients than in matched controls. The increment of binding capacity with sodium was similar in controls and diabetic patients so that maximal binding capacity in a NaCl system was 1.7 +/- 0.3 in controls and 3.64 +/- 0.5 in diabetic patients (p less than 0.025). Half maximal furosemide binding by Tamm Horsfall glycoprotein occurred at 1.4 +/- 0.2 mmol Na/l in controls and 0.52 +/- 0.12 in diabetic patients (p less than 0.01). Abnormal radiofurosemide binding of Tamm Horsfall glycoprotein of diabetic patients may be the consequence of abnormal postribosomal modification of the glycoprotein which is synthesized in an insulin- and glucose-sensitive nephron segment.

Adult↗
PubMed1985

Demonstration and characterization of 1,25-dihydroxyvitamin D3 receptors in basal cells of epidermis of neonatal and adult mice.

Nuclear and cytosolic receptors for 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were demonstrated in the epidermis of neonatal and adult mice. The macromolecular binding protein sedimented at 3.5 S (sucrose density gradient) and was distinct from the 6.0 S binding protein for 25-hydroxycholecalciferol [25(OH)D3]. Analysis at different ionic strengths suggested the presence of unoccupied nuclear receptors. Digestion with proteases or nucleases, respectively, and inactivation with alkylating agents demonstrated that the binding macromolecule is a protein with SH groups at the active site. Binding of 1,25(OH)2D3 was specific and reversible. In neonatal mice KD was 1.6 X 10(-10) M for both cytosolic and nuclear fractions, binding capacity was 54 fmol/mg protein in the cytosolic and 108 in the nuclear fractions, respectively. The phenotypic expression of the 1,25(OH)2D3 receptor (dissociation constant, binding capacity) was identical in neonatal and adult epidermis. Half maximal displacement of 1,25(OH)2D3 was achieved with an 80-fold and 200-fold molar excess of 25(OH)D3 and 1-alpha-hydroxycholecalciferol [1(OH)D3], respectively. Using Percoll density gradient centrifugation, 1,25(OH)2D3 receptors could be localized in the basal cell fraction. DNA cellulose chromatography with 1,25(OH)2D3 receptor elution from DNA at 0.25 M KCl (linear gradient) points to a possible role in gene transcription. In mouse primary epidermal cell cultures, 1,25(OH)2D3, but not 25(OH)D3, 24,25(OH)2D3, and 1(OH)D3 influenced [3H]thymidine incorporation (at physiological concentrations); the magnitude of change depending on the concentration of 1,25(OH)2D3 and the time of incubation. These data demonstrate that skin is a target organ for the active vitamin D secosterol.

Animals↗
PubMed1985

Myocardial hypertrophy in rats with renal insufficiency.

Increased defatted dry wt of the heart and increased heart calcium content were observed in subtotally nephrectomized male Sprague-Dawley rats compared with sham-operated pairfed controls. Increased heart wt contrasted with no change of the weight of viscera (liver, spleen) and markedly decreased weight of striated muscle. Heart wt was unchanged after 5 days of renal insufficiency, but significantly increased after 14 or 21 days. Increased heart wt persisted despite effective beta adrenoreceptor blockade (2 X 10 mg metroprolol/kg/day i.p.) or effective alpha-1-adrenoreceptor blockade (2 X 2 mg prazosin/kg/day i.p.). Increased heart wt was also demonstrable despite normalization of basal blood pressure (intraarterial blood pressure measurement in conscious animals): blood pressure was lowered in one series with hydralazine/nadolol in drinking water (calculated to deliver 20 and 2 mg/kg/day, respectively) and in another series with furosemide in drinking water (15 mg/kg/day) combined with metoprolol (2 X 10 mg/kg/day i.p.). Increased heart wt was also noted despite correction of anemia by blood transfusion (Hct greater than 40%) and after parathyroidectomy in animals kept eucalcemic with high dietary calcium. Micromorphometry of left ventricular myocardium in perfusion-fixed tissue showed no significant change of the relative proportion of connective tissue and myocardial fibers. Myocardial isomyosin pattern was changed with an increase of fast-migrating V1 isomyosin in animals with renal insufficiency compared to sham-operated pairfed controls.

Adenosine Triphosphatases↗
PubMed1985

125I-Angiotensin II binding to human blood cells.

The binding of 125I-angiotensin II to human blood cells was investigated. Blood was drawn from healthy volunteers and platelets prepared with minimal contamination of red cells and white blood cells (less than 0.1%). Using thin layer chromatography, degradation of 125I-angiotensin II by platelets could be demonstrated in the presence of various enzyme inhibitors. However, when incubated with 1 mM diisopropylfluorophosphate (DFP) or 1 mg/ml bacitracin, no breakdown of 125I-angiotensin II could be detected. The amount of specifically bound 125I-angiotensin II increased linearly with the number of cells per tube. Binding reached a plateau within 90-120 min at 37 degrees C, and was stable thereafter. Specific binding was reversible. No binding could be detected at 4 degrees C. Specific binding of 125I-angiotensin II was saturable. Scatchard analysis of binding by platelets of healthy volunteers revealed one class of binding sites with an apparent Kd of 127 +/- 16 pM and a maximal binding capacity of 7.9 +/- 1.5 binding sites per cell. Competitive displacement of 125I-angiotensin II binding by angiotensin II-analogues showed a rank order of effectiveness. Unrelated peptides, e.g. bradykinin, vasopressin and enkephalin, did not displace specifically bound angiotensin II. Human mononuclear leucocytes were prepared by a Ficoll-isopaque gradient. However, these cells could not be used for studies of specific binding, since enzymatic degradation of 125I-angiotensin II could not be prevented despite addition of various enzyme inhibitors. Time-dependent uptake of 125I-angiotensin II showed no stable plateau. Thus our study shows specific binding of 125I-angiotensin II to human platelets.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Digitalis in chronic renal insufficiency.

Cardiac dysfunction is common in patients with terminal renal failure. However, no consensus has been reached with respect to the indications for digitalis therapy. Depression of myocardial contractility may occur as a result of circulating toxic factors, parathyroid hormone, and altered catecholaminergic responsiveness. On the other hand, paradoxical positive inotropic effects have been observed possibly as a result of a circulating natriuretic factor (an endogenous digitalis analogue) which inhibits Na,K-ATP'ase. Pharmacokinetics and pharmacodynamics of digitalis steroids are altered in uremia. Elimination half-lives of strophanthin and digoxin are prolonged, whereas the elimination half-life of digitoxin is unchanged. Altered protein binding and volume of distribution have been noted. Despite its long elimination half-life, most nephrologists favor administration of digitoxin because of its insensitivity to changes in renal function.

Animals↗
PubMed1985

Treatment of hypertension in dialysis patients.

Hypertension is common in hemodialyzed patients and constitutes an important cardiovascular risk factor. Fluid retention, inappropriate stimulation of the renin-angiotensin system, sympathetic overactivity and changes of vessel wall structure have been shown to be important factors in its pathogenesis. It has been claimed that hemofiltration permits a better control of hypertension in the interdialytic interval, although the evidence is not perfectly convincing; blood pressure tends to be lower with continuous ambulatory peritoneal dialysis. While fluid withdrawal and - within certain limits - adjustment of dialysate sodium concentration constitutes a primary line of therapy, antihypertensive medication is necessary in approximately 20% of patients. Specific problems with dialysis patients are cumulation of drugs (some cardioselective beta-blockers, alpha-methyldopa, captopril), altered dose-response relationship (diuretics) and particularly interaction with cardiovascular stability during fluid withdrawal.

Adolescent↗
PubMed1985

Antimicrobial therapy in dialysis patients. I. Penicillins and cephalosporins.

Antibiotic therapy, using penicillins or cephalosporins, is frequently required in patients on maintenance hemodialysis. Points to consider are dose adjustment for drugs which are excreted via the kidney, drug dialysability, and cumulation with frequent occurrence of side reactions, neurotoxicity and bleeding being the clinically most important ones. For third-generation cephalosporins with N-methylthiotetrazole side chain, impaired intrahepatic vitamin K metabolism may cause problems of hemostasis which can be avoided by dose adjustment and prophylactic administration of vitamin K1.

Bacterial Infections↗
PubMed1985

Response of alkaline phosphatase to zinc repletion in hypozincemic hemodialysis patients.

The response of serum alkaline phosphatase (AP), a zinc-dependent metalloenzyme, to zinc administration via the dialysate (400 micrograms/l) was examined in 14 hypozincemic (less than 30th percentile of dialysis patients) hemodialysis patients and in 14 placebo-treated matched dialysis control patients. Plasma zinc and serum AP were measured three times: prior to, once weekly during (5 weeks), and 2 weeks after addition of zinc to the dialysate. The serum zinc levels remained stable in placebo-treated controls (initial 87.7 +/- 12.5; final 78.6 +/- 8.3 micrograms/dl) and increased in zinc-treated patients (initial 76.4 +/- 8.3; 5th week 96.9 +/- 13.3; 2 weeks after zinc withdrawal 82.3 +/- 12.2 micrograms/dl). There was a slight increase of AP with time in placebo controls (initial 90.2 +/- 26.5; 5th week 100 +/- 29 U/l) and a more pronounced increase in zinc-treated patients (initial 90.8 +/- 19.9; 5th week 113 +/- 20.9 U/l). The difference between the two groups was marginally significant (p less than 0.05; analysis of variance). It is concluded that zinc repletion via dialysate with documented increase of serum zinc levels in initially hypozincemic dialysis patients causes a reversible increase of serum AP. The result is compatible with some tissue zinc deficiency in hypozincemic dialysis patients.

Adult↗
PubMed1985

Evidence for macrophage activation in dialysis patients exposed to silicone filing.

Spleen cell suspensions of 2 dialysis patients with hepatosplenomegaly and pancytopenia were studied in vitro. Spleen cells of a cadaver kidney donor were studied as control. In spleen macrophages of the patients, silicone particles could be demonstrated with TEM and electron microprobe analysis. Under basal conditions and after stimulation with zymosan and concanavalin A, release of PGE2, TXB2 and 6-keto-PGF1 alpha from patient cells was higher than control cells. This anecdotal observation parallels previous animal studies and suggests that loading of human macrophages with foreign material particles activates arachidonic acid metabolism.

Adult↗