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R Re

Publications and source records attributed to R Re.

At least 37 records · Page 2Linked to original sources
PubMed1984

Effect of angiotensin II on RNA synthesis by isolated nuclei.

Peptide hormones are known to bind to cell surface receptors as the first step in the generation of their effects on target tissues. However, it remains uncertain whether internalized hormone might also play a role in the production of longterm or trophic effects of peptide hormones. Because the peptide hormone angiotensin II appears to be internalized by target cells, we studied the effect of this peptide on isolated hepatic nuclei. At both 5 X 10(-7)M and 5 X 10(-9)M, angiotensin II significantly increased RNA synthesis. This effect was not mimicked by Sar1-Ala8-angiotensin II (saralasin) or the unrelated nonapeptide teprotide.

Angiotensin II↗
PubMed1984

A simplified radioimmunoassay for physiologically active angiotensin peptides [(1-8) octa- and (2-8) heptapeptides].

The availability of a sensitive and highly specific rabbit antiserum and the development of a peptide-extraction method employing glass beads permitted the evolution of a rapid reliable radioimmunoassay that measures the sum of the concentration of angiotensin II and its active metabolite, angiotensin III. At a dilution of 1:32,000 the antiserum is capable of measuring 1 fmol (1 pg) of angiotensin II. Cross reactivities of this antiserum, taking angiotensin II as 1.0, are: angiotensin III, 0.75; angiotensin-(3-8) hexapeptide, 0.11; angiotensin I, 0.006; angiotensin-(1-14) tetradecapeptide, 0.0001. The recovery of angiotensin II added to hormone-free plasma was 73 +/- 2% [mean +/- standard deviation (SD), n = 20]. When 0.9 ml of plasma was extracted, the minimal concentration of angiotensin II and III that could be quantified was 4 fmol/ml. When larger volumes of plasma were extracted, sensitivity was enhanced. Plasma blanks were zero. Intra-assay variability was 7.6% SD and interassay variability was 11.7% SD. Angiotensin II and III concentration in venous plasma of normal volunteers on an ad libitum diet was 15 +/- 8 fmol/ml (mean +/- SD, range less than 4 to 35 fmol/ml). The plasma of a patient with primary aldosteronism had an unmeasurable value (less than 4 fmol/ml). Posture, converting enzyme inhibition, and renal artery stenosis resulted in expected changes of angiotensin concentration.

Angiotensin II↗
PubMed1983

Selectivity of angiotensin II antisera.

A significant problem in the immunoassay of angiotensin II is the cross-reactivity of most available antisera with the peptide's metabolic products, (des-Asp1)-angiotensin II and (des-Asp1.Arg2)-angiotensin II. In order to attempt to generate antisera of greater selectivity, a variety of conjugates between angiotensin II or derivative peptides and carrier proteins were examined as immunogens with the aim of generating antisera that would selectively identify the amino terminal region of the peptide. Selectivity for the amino terminus was achieved by either (1) immunization with N-acetylated angiotensin II-amide which had been coupled to rabbit serum albumin by its carboxy terminus, or (2) immunization with angiotensin-(1-7)-heptapeptide which was randomly coupled to thyroglobulin. The antisera produced with the N-acetylated immunogen cross-reacted with the unacetylated ligand (Asn1-Val5)-angiotensin, but did not recognize the human hormone (Asp1,Ile5)-angiotensin. Carboxy-terminal coupling of angiotensin without N-acetylation did not induce selectivity for the amino terminus, nor did a conjugate which was linked to the carrier protein via a diazo bond to His6 of the peptide. These findings may be explained by the fact that N-acetylated angiotensin II resists degradation by amino peptidases and thus retains its structure in the immunogen and by the fact that the (1-7)-heptapeptide has lost the immunodominant carboxy-terminal epitope, thus emphasizing the desired amino terminal determinant.

Angiotensin II↗
PubMed1982

Renin synthesis by canine aortic smooth muscle cells in culture.

Angiotensin-I generating activity has been detected in homogenates of arterial tissue but it remains unclear whether this enzymatic activity results from the presence of renin itself or from the action of other proteases such as cathepsin D. In an assay system employing anephric dog plasma as substrate and buffered to pH 7.4, we detected angiotensin-I generating activity in homogenates of canine aortic smooth muscle cells. This enzymatic activity was in large part inhibitable by renin-specific antisera raised to pure canine renal renin. Immunofluorescent study of cultured arterial smooth muscle cells was also performed using renin specific antiserum. Granular cytoplasmic immunofluorescence was detected when specific antirenin serum was used but not when preimmune serum was employed. The addition of pure canine renin to the renin antiserum during staining suppressed the granular immunofluorescence confirming the specificity of staining. Finally, biosynthetic radiolabelling studies were performed. Immunoprecipitation of newly synthesized proteins with antirenin serum and staphylococcal protein A followed by gel electrophoresis and autoradiography demonstrated the synthesis of an immunoreactive protein with the molecular weight of renin. Pretreatment of the antirenin serum with pure canine renin resulted in the disappearance of this immunoreactive protein band. Thus these studies provide multiple lines of evidence to indicate the in situ synthesis of renin by vascular smooth muscle cells.

Animals↗
PubMed1982

Pulmonary hypertrophic osteoarthropathy in a child with late-onset agammaglobulinemia.

A case of hypertrophic osteoarthropathy is described in an 8-year-old child with late-onset agammaglobulinemia, bronchiectasis and clubbing of the fingers and toes. The child presented with pain of recent onset in the legs, ankles, and knees and a diagnosis of hypertrophic osteoarthropathy was made on the basis of the radiologic findings. Therefore the differential diagnosis of bone and joint pain in agammaglobulinemic subjects must take into account hypertrophic osteoarthropathy.

Agammaglobulinemia↗
PubMed1982

Studies on two novel angiotensin II actions.

Animal data suggest that angiotensin II may directly affect renal sodium retention independent of aldosterone (4,6). Additionally there is evidence to suggest that the hormone can stimulate protein synthesis in a variety of tissues and that indeed it may be a vasculotoxin (5,7). We describe here experiments designed to elucidate the role of angiotensin II in renal sodium retention in normal man. Additionally we present preliminary evidence suggesting that unlike the rapid sodium retaining effect, some delayed (trophic) actions of the hormone may be generated by a hitherto unappreciated mechanism.

Adult↗
PubMed1981

Golgi-ANAE positivity in leukemic blast cells: a possible T-suppressor cell leukemia.

Different patterns of acid alpha-naphthyl-acetate esterase (ANAE) positivity in lymphocytes have been related to distinct functional lymphocyte subpopulations. A case of T-ALL with a cytochemical and immunological phenotype consistent with a T-suppressor cell leukemia is reported. In particular a specific pattern of Golgi-ANAE positivity is probably characteristic of TG cells, which include a subset with suppressor function.

Bone Marrow Cells↗
PubMed1980

Dissociation of renin--aldosterone and renal prostaglandin E during volume expansion induced by immersion in normal man.

The relationship of the renin--angiotensin--aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 +/- 7%) and plasma aldosterone concentration (55 +/- 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin--aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

Adult↗
PubMed1978

Inhibition of angiotensin-converting enzyme for diagnosis of renal-artery stenosis.

To determine its utility as an aid in diagnosis of renovascular hypertension, we administered nonapeptide converting-enzyme inhibitor (CEI) (which inhibits conversion of angiotensin I to angiotensin II) (0.25 mg per kilogram) to 14 unselected hypertensive patients undergoing bilateral renal-vein catheterization. In seven (Group I) predominantly unilateral disease was discovered by angiography (renal-artery stenosis in six and hydronephrosis in one); in the remaining seven (Group II) no rennal-artery abnormality was found. In Group I, mean (+/- S.E.) ratio of involved to uninvolved renal-vein plasma renin activity (PRA) increased from 2.94 +/- 0.91 before to 8.36 +/- 2.94 after CEI (P less than 0.01). In Group II, the ratio (of the initially higher to the lower side) was 1.99 +/- 0.49 before and 1.17 +/- 0.07 after CEI (P greater 0.02). Post-CEI PRA was predicted by pretreatment PRA. Mean blood pressure fell in both groups after CEI, and the decrement was predicted by pre-CEI PRA. These data suggest that CEI can be of use at the time of renal-vein catheterization, serving to increase diagnostic accuracy by increasing the difference in PRA between the two sides when there is unilateral disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1978

Volume as a determinant of plasma aldosterone in anephric man.

Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI), produces a prompt and profound suppression of plasma renin activity (PRA) and plasma aldosterone concentration (PA) without concomitant alterations in serum sodium and potassium concentrations. The NI model was utilized to assess the responsiveness of PA to volume expansion in 12 anephric subjects. The patients were studied on 2 occasions, 48 h after their last dialysis: during a seated control study (7 of the patients) and during 3 h of NI (all 12 patients). The conditions of seated posture and time of day were identical. Blood for PRA, PA, and cortisol was obtained at 30-min intervals for 5 h. PRA was undetectable in all patients. NI failed to alter PA. Plasma cortisol declined progressively throughout NI; serum potassium concentration remained unchanged. An identical NI study in normal subjects suppressed PA by 60%. These data demonstrate that when plasma composition and posture are maintained constant, marked central hypervolemia does not alter PA in anephric man. The present findings support the role of the renin-angiotensin system as the prepotent mediator of volume-induced changes in PA.

Adult↗
PubMed1977

Effect of ethane-1-hydroxy-1,1-diphosphonate (EHDP) on the ultrastructure of parathyroid glands and plasma immunoreactive parathyroid hormone in pregnant cows fed a low calcium diet.

The long term (70 days) effects of administering ethane-1-hydroxy-1,1-diphosphonate (EHDP) (4 mg. per kg. per day) on parathyroid function was investigated in pregnant cows fed a low calcium diet. Serum calcium and phosphorus were significantly lower at parturition and postpartum in EHDP-treated cows compared to pregnant control cows fed the low calcium diet. Plasma immunoreactive parathyroid hormone levels were similar prepartum, at parturition, and postpartum in cows administered EHDP and control cows. Immediately available calcium reserves were greater preparation in control cows than in cows receiving EHDP as indicated by a more rapid rate of return of serum calcium toward normal levels following ethylenediaminetetraacetic acid (EDTA)-induced hypocalcemia approximately 10 days prepartum. EHDP-treated cows responded to the hypocalcemic challenge with similar changes in plasma immunoreactive parathyroid hormone levels as in control cows; however, urinary hydroxyproline excretion increased at certain intervals only in control cows. Ultrastructurally, chief cells in parathyroid glands of both groups of cows were in an active stage of the secretory cycle with well developed organelles concerned with hormonela synthesis. Chief cells in cows administered EHDP were degranulated and contained fewer secretory granules in response to the hypocalcemia than those in control cows. Chief cells in EHDP-treated cows often had prominent perinuclear accumulations of microfilaments, scattered vacuolated mitochondria, and lysosomal bodies in the cytoplasm. Thyroid C-cells were densely granulated and thyroid calcitonin content was similar in both groups of cows. The principal defect in calcium homeostasis of EHDP-treated cows appeared to be an impairment both in bone calcium mobilization and bone matrix catabolism in response to the secretion of parathyroid hormone. In vitro uptake of 45Ca by duodenal mucosa and urinary excretion of cyclic adenosine monophosphate were similar in both groups of cows. The ability of the parathyroid glands to synthesize and secrete parathyroid hormone in response to hypocalcemia induced either by EDTA or associated with parturition was not impaired by the administration of EHDP.

Animals↗
PubMed1977

Effect of dichloromethane diphosphonate on calcium homeostatic mechanisms in pregnant cows.

The administration of 4 mg/kg/day of dichloromethane diphosphonate (Cl2MDP) subcutaneously to pregnant cows fed a low-calcium diet significantly reduced bone resorption as indicated by microradiographic evaluation of endosteal surfaces of cross sections of ribs. Plasma parathyroid hormone levels were similar between Cl2MDP-treated and control cows prepartum, during EDTA infusions, and near parturition. Ultrastructurally, chief cells of the parathyroid glands of both groups of cows were in the active stage of the secretory cycle. The chronically stimulated chief cell from cows administered Cl2MDP had a large cytoplasmic area containing many lipofuscin granules and lysosomal bodies and a few secretory granules near the large Golgi apparatus or aligned along the plasma membrane. Uptake of calcium 45 by the duodenal mucosa incubated in vitro was greater in Cl2MDP-treated cows compared to control cows. The administration of Cl2MDP significantly reduced rapidly mobilization calcium reserves. Following an intravenous EDTA infusion and the spontaneous calcium drain associated with parturition and the beginning of lactation, Cl2MDP-treated cows developed severe hypocalcemia. The rapid mobilization of calcium reserves in cows administered Cl2MDP prepartum was impaired mainly because of diminished resorption of bone despite adequate parathyroid hormone secretion in response to severe postpartal or EDTA-induced hypocalcemia.

Animals↗