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H Schmidt-Gayk

Publications and source records attributed to H Schmidt-Gayk.

At least 55 records · Page 3Linked to original sources
PubMed1996

Abnormal expression and regulation of vitamin D receptor in experimental uremia.

The low concentration of the biologically active metabolite of vitamin D, namely 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3), is critical to the pathogenesis of secondary hyperparathyroidism in chronic renal failure. The actions of 1,25(OH)2D3 are mediated through binding to a cellular receptor protein, the vitamin D receptor (VDR). In order to further investigate expression and regulation of VDR in uremia, we measured specific [3H]-1,25(OH)2D3 binding capacity and VDR mRNA concentration in intestinal mucosa and in parathyroid glands of subtotally nephrectomized rats (Nx) and compared Nx to sham-operated rats with normal kidney function (Intact). Intestinal [3H]-1,25(OH)2D3 binding capacity in short-term Nx (6-10 days after nephrectomy) was 663 +/- 114 fmol/mg protein; it was 517 +/- 34 in Intact (p = 0.06, n = 6 experiments). Intestinal VDR mRNA concentration was comparable between Nx and Intact. Specific 1,25(OH)2D3 binding capacity in parathyroid glands was higher in Nx (195 +/- 9 fmol/mg protein) than in Intact (116 +/- 14 fmol/mg protein, n = 5, p < 0.05). The affinity of the VDR for 1,25(OH)2D3 (KD) did not change in Nx. The 1,25(OH)2D3 binding capacity in intestinal mucosa of more long-term uremic animals (14-16 weeks after subtotal Nx) was 519 +/- 32 fmol/mg protein versus 349 +/- 31 in Intact (n = 3, p < 0.01). Parathyroid VDR was 171 +/- 9 fmol/mg protein in long-term Nx and 125 +/- 3 in Intact (p < 0.01). These results were confirmed when 1,25(OH)2D3 binding capacity in uremic rats with hereditary polycystic kidney disease was compared to control rats with normal kidney function (757 +/- 54 fmol/mg protein versus 495 +/- 59 in intestinal mucosa, p < 0.05; 273 +/- 48 versus 104 +/- 27 in parathyroid glands, p < 0.05). In parallel to changes in intestinal 1,25(OH)2D3 binding capacity, 1,25(OH)2D3-mediated stimulation of intestinal 25(OH)D3-24-hydroxylase activity was significantly higher in long-term subtotally Nx (1.43 +/- 0.06 pmol 24,25-dihydroxyvitamin D3/mg protein) than in sham-operated normal rats (1.04 +/- 0.10, p < 0.05). Administration of 1,25(OH)2D3 to sham-operated normal rats resulted in an increase of 1,25(OH)2D3 binding capacity by 20-40% in intestinal mucosa and by 40-50% in parathyroid glands. In contrast, 1,25(OH)2D3 caused down-regulation of mean 1,25(OH)2D3 binding capacity in short-term Nx by 38% in intestinal mucosa (p < 0.01) and by 43% in parathyroid glands (p < 0.01). In long-term Nx, mean 1,25(OH)2D3 binding capacity was reduced by 20% in intestinal mucosa (p < 0.05) and by 22% in parathyroid glands (p < 0.01). After prolonged exposure to 1,25(OH)2D3 for 6 weeks, intestinal 1,25(OH)2D3 binding capacity was markedly down-regulated in uremic rats (43% versus vehicle-treated animals p < 0.05). Taken together, our results provide evidence for abnormal expression and regulation of VDR in experimental uremia. This may be relevant for responsiveness to 1,25(OH)2D3 in renal insufficiency.

Animals↗
PubMed1996

Control of pulsatile and tonic parathyroid hormone secretion by ionized calcium.

To investigate the effect of changes in ionized calcium on instantaneous PTH secretion, we examined seven young healthy volunteers by 1-min blood sampling under conditions of normo-, hypo-, and hypercalcemia. After a baseline period of 75 min, ambient ionized calcium was either increased or decreased by 0.2 mmol/L for 105 min by clamped infusion of calcium gluconate or sodium citrate. The characteristics of PTH secretion were analyzed by a deconvolution technique, accounting for subject-specific plasma PTH disappearance half-life, as measured during the first 15 min of calcium infusion (range, 2.04-2.93 min). The process regularity of pulsatile PTH secretion was evaluated by an approximate entropy statistic. Under baseline conditions, 32% of total PTH secretion was released in a pulsatile fashion, with a burst frequency of 6.9 +/- 0.8 h-1 and a PTH mass per burst of 2.6 +/- 0.9 pmol/L. The remaining 68% of total secretion was attributed to tonic hormone release. During the initial 30 min of induced hypocalcemia, pulsatile secretion increased by 1140%, whereas tonic secretion did not change. The preferential increase in pulsatile PTH secretion was mediated by a combined rise in burst frequency and mass released per burst. During subsequent steady state hypocalcemia, the tonic secretion rate increased (255% of baseline), whereas burst frequency and burst mass decreased (to 103% and 189% of the baseline values), restoring the baseline ratio of tonic to pulsatile PTH secretion. The regularity of PTH release increased during steady state hypocalcemia. During hypercalcemia, tonic secretion, burst mass, and burst frequency decreased by 75%, 82%, and 32%, respectively, and remained constant throughout the clamp period. We conclude that acute hypocalcemia elicits an immediate pulsatile and a delayed tonic secretory response of the parathyroid gland with increased regularity of PTH release. Acute hypercalcemia suppresses both the pulsatile and the tonic component of PTH secretion.

Adult↗
PubMed1995

Solid-phase competitive luminescence immunoassay for lysozyme in faeces.

We have developed a new simple solid-phase luminescence immunoassay (LIA) for the determination of faecal lysozyme. The assay utilises a polyclonal capture antibody coated to polystyrene beads and acridinium ester-labelled human lysozyme as tracer. Samples are incubated with polystyrene beads and tracer overnight at 4 degrees C. After a thorough washing step, emitted light is measured by an automated luminometer for 2 seconds. The standard curve uses five standards ranging from 0.025 to 6.4 mg/l. The method has a sensitivity of 0.02 mg/l. Dilution recoveries for three samples were 88, 104 and 108%. Intraassay coefficients of variation (CV, n = 24) were 10.1% and 11.7% for a healthy control and a patient sample; interassay CV (n = 16) were 6.7% and 13.1% for the same healthy control but another patient sample. The normal range of faecal lysozyme in 80 healthy controls was found to be 0.02-1 mg/l (97.5 percentile) with a median of 0.28 mg/l. Fifty-three patients with Crohn's disease had faecal lysozyme values ranging from 0.16 to 100.7 mg/l with a median of 1.75 mg/l, and 30 patients with ulcerative colitis showed levels between 0.09 and 118 mg/l with a median of 1.11 mg/l. The assay has proved useful for differentiating healthy individuals from those with inflammatory bowel disease and might be a valuable tool for diagnosing or evaluating inflammatory bowel disease.

Adolescent↗
PubMed1995

Low-dose calcitriol prevents the rise in 1,84-iPTH without affecting serum calcium and phosphate in patients with moderate renal failure (prospective placebo-controlled multicentre trial).

BACKGROUND: Higher doses of calcitriol are effective in lowering markedly elevated 1,84 PTH levels of patients with renal secondary hyperparathyroidism. It has not been established, however, whether prophylactic administration of low doses of calcitriol prevents an increase of 1,84 PTH without causing side-effects, i.e. hypercalcaemia, hypercalciuria, or hyperphosphataemia. STUDY DESIGN: We carried out a placebo-controlled, double-blind prospective multicentre trial over 12 months in 45 patients with mild to moderate renal failure. Criteria for inclusion were S-creatinine 1.4 mg/dl and 1,84 PTH > 6 pmol/l (normal 6). Calcitriol 0.125 microgram/day per os was compared with placebo. The patients received calcium carbonate per os if serum P exceeded 1.7 mmol/l. RESULTS: Baseline 1,84 iPTH concentrations were not significantly different, i.e. 14.0 pmol/l (6.7-63.3) on placebo vs 16.2 (6.85-82.0) on calcitriol. Intention to treat analysis revealed a significant difference of final 1,84 iPTH, i.e. 27.8 (4.2-68.5) on placebo vs 18.2 (4.45-75.5) on calcitriol. On post-hoc analysis the difference was even more pronounced at S-creatinine concentrations above 3 mg/dl. S-calcium, S-phosphate, and urinary excretion of calcium did not change significantly on either placebo or on calcitriol. There were no episodes of hypercalcaemia or hyperphosphataemia. There was no significant difference of final S-creatinine or change in S-creatinine between placebo and calcitriol. One patient on calcitriol and two on placebo progressed to terminal renal failure. Bone alkaline phosphatase as a non-invasive index of bone metabolism was not decreased to subnormal levels. CONCLUSION: The results document that a therapeutic window exists in patients with moderate renal failure and elevated of 1,84 iPTH, where low-dose calcitriol (0.125 microgram/day) prevents the increase in 1,84 iPTH without causing side-effects. This observation suggests that the parathyroid is more sensitive to calcitriol than intestine and bone.

Adult↗
PubMed1995

Noninvasive parameters of bone metabolism.

Markers of bone formation determined in serum include alkaline phosphatase, bone-specific alkaline phosphatase, osteocalcin [bone gamma-carboxyglutamic acid peptide (BGP) and procollagen type I carboxyterminal propeptide. Recently, advances have been made in the immunoassay of bone-specific alkaline phosphatase. This is a marker for osteoblastic activity; it is very stable and is not primarily dependent on kidney function because it is degraded in the liver. BGP is not specific for bone formation because it increases in serum during bed rest (which involves increased bone resorption), and it is not stable. Furthermore, the elimination of BGP is dependent on glomerular filtration rate. Procollagen type I carboxyterminal propeptide is not as sensitive as bone-specific alkaline phosphatase because it increases less in women after the menopause. Urinary pyridinoline and deoxypyridinoline determined by high-performance liquid chromatography are regarded as the best methods for measuring bone resorption. These might be replaced by type I collagen crosslinked N-telopeptide or CrossLaps in the future in laboratories not equipped with a high-performance liquid chromatography system. Serum markers of bone resorption are currently under investigation. An immunoassay for the tartrate-resistant acid phosphatase in serum should be a very promising tool for the quantification of bone resorption.

Animals↗
PubMed1995

Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy.

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

The long-acting somatostatin analogue octreotide alleviates symptoms by reducing posttranslational conversion of prepro-glucagon to glucagon in a patient with malignant glucagonoma, but does not prevent tumor growth.

A 52-year-old female with metastatic glucagonoma secreting glucagon and chromogranin A was treated with the somatostatin analogue octreotide for 2 years without any additional tumor-reducing interventions. Before therapy plasma glucagon was above 8 micrograms/l (normal < 0.2) and within 2 days 3 x 200 micrograms octreotide daily suppressed plasma glucagon to 2.2-2.5 micrograms/l. Concomitantly, chromogranin A dropped from 0.85 mg/l (normal < 0.1) to 0.2. After 3 weeks the preexisting disabling necrolytic migratory erythema had vanished completely, and weight loss was temporarily stopped. During therapy chromogranin A and plasma glucagon rose, exceeding pretreatment levels after 3 and 14 months, respectively. After 1 year the erythema recurred, responding only transiently to increasing doses of octreotide. The patient died after 2 years of therapy of tumor cachexy despite very high doses of octreotide (4 x 600 micrograms/day). Throughout treatment octreotide did not prevent tumor growth, as demonstrated by computed tomography and sonography. Determination of immunoreactive glucagon before and during octreotide therapy in fractions of plasma samples subjected to gel chromatography revealed a reduction in the ratio of glucagon to preproglucagon from 1.83 (before) to 0.56 (during therapy), indicating inhibition of posttranslational processing of preoproglucagon by octreotide, thereby reducing circulating bioactive glucagon. In summary, octreotide induced a remission of clinical symptoms by inhibiting posttranslational conversion of preproglucagon to glucagon but did not prevent tumor growth. Therefore, octreotide is a valuable therapy for rapid relief of clinical symptoms, thereby improving the possibilities for other tumor-reducing therapies.

Cell Division↗
PubMed1994

Comparison of intermittent and continuous oral administration of calcitriol in dialysis patients: a randomized prospective trial.

Intermittent bolus administration of calcitriol--i.e., 1,25-dihydroxycholecalciferol or 1,25-(OH)2D3--is highly efficacious in dialysis patients. In experimental studies, intermittent administration of calcitriol is superior to continuous administration in suppressing preproparathyroid hormone (PTH) mRNA and circulating PTH concentrations. In a randomized, prospective, open multicenter trial 45 dialysis patients with elevated 1,84-iPTH (> or = 20 pmol/l, normal 1-6 pmol/l) levels were randomly allocated to daily administration of 0.75 microgram calcitriol (continuous) or twice weekly administration (intermittent); the two protocols provided an identical total weekly doses of 5.25 micrograms calcitriol. Patients were dialyzed with a dialysate Ca concentration of 1.75 mmol/l and had oral CaCO3 or Ca acetate. 1,84-iPTH (immunoradiometric assay) and serum Ca and Pi levels were measured weekly. At the beginning of the study, the median 1,84-iPTH value was 37 pmol/l (range 20-115) in the intermittent versus 36 pmol/l (range 21-72) in the continuous calcitriol group. After 2 weeks, the median 1,84-iPTH level was 18.5 pmol/l (range 1.4-106) versus 18 pmol/l (range 1.2-48). After 12 weeks, 11 of 21 of the patients in the intermittent and 18 of 24 patients in the continuous group had reached the treatment goal, i.e., 1,84-iPTH < or = 10 pmol/l without hypercalcemia or hyperphosphatemia. There were seven episodes of hypercalcemia (> 2.7 mmol/l) in the intermittent versus two in the continuous group; the mean peak Ca level was 2.8 mmol/l (range 2.76-3.0) versus 2.9 mmol/l (range 2.74-3.06). There were 21 versus 17 episodes, respectively, of hyperphosphatemia (> 2.2 mmol/l).

Administration, Oral↗
PubMed1994

Markers of bone metabolism during short-term administration of thyroxine in healthy volunteers.

We investigated the influence of L-thyroxine (L-T4) treatment over 3 weeks on biochemical markers of bone turnover in 12 healthy young men (age 25.6 +/- 1.4 years, BMI: 22.6 +/- 2.5 kg/m2). Serum parameters indicating bone formation [bone Gla protein (BGP), carboxyterminal propeptide of type I procollagen (PICP), and bone-specific alkaline phosphatase (BAP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and the urinary excretion of pyridinoline (Pyr) and deoxypyridinoline (D-Pyr)] were measured before and after three weeks of treatment with 300 micrograms L-T4/d. T3 and T4 significantly increased and TSH decreased to almost undetectable levels even when measured with a third generation TSH assay. Markers of bone formation showed variable responses with a small but significant increase in BGP but not in PICP or BAP. In contrast, all parameters of bone resorption increased significantly with a good correlation between D-Pyr excretion and the serum parameter ICTP (r = 0.78, p < 0.0001). These changes in bone-turnover markers were not necessarily paralleled by comparable increments of other markers of tissue thyrotoxicosis (SHBG, pulse rate, VO2), suggesting a variability in tissue sensitivity. These rapid responding parameters, especially in the easily obtainable serum parameter ICTP, might be valuable tools in the evaluation of several states of thyroxine excess.

Adult↗
PubMed1994

Single-dose oral calcitriol and changes of plasma 1,84iPTH in uremic children.

Both intravenous and oral 1,25(OH)2 D3 pulse therapy are effective in decreasing iPTH in patients with chronic renal failure. In order to understand why intermittent application of calcitriol is effective, we investigated 10 children with advanced renal failure (4 female, 6 male; median age 6.5 [3-16] years; body surface area 0.58-1.57m2; CCR 7 [5-47] mL/min/1.73m2) with elevated baseline concentrations of 1,84iPTH (median 63.5 [9.4-300] pmol/L). After a standard dose of 2 micrograms calcitriol per os (equal to 1.27-3.45 micrograms/m2), serum 1,25(OH)2D3 concentrations increased. The peak concentration occurred after 6 h (3-12), and 1,25(OH)2D3 serum levels returned to baseline by 48 h. 1,84iPTH concentrations were significantly suppressed by 6-72 h. The median maximal decrease was 51.4% of baseline (22.3%-74%). The decrement was a function of baseline 1,84iPTH, but not of 1,25(OH)2D3 serum peak concentration, area under the curve, body surface area, or change in ionized serum calcium. We conclude: (i) oral 1,25(OH)2D3 has a prolonged (up to 72 h) suppressive effect on 1,84iPTH concentrations in uremic patients, and (ii) the wide interindividual variation in suppression of 1,84iPTH was not explained by the kinetics of 1,25(OH)2D3 concentration, which implies that additional factors influence the 1,84iPTH response to 1,25(OH)2D3.

Administration, Oral↗
PubMed1994

Influence of long-term erythropoietin treatment on plasma levels of calcium-phosphate related hormones in haemodialyzed uraemic patients.

Exacerbation of secondary hyperparathyroidism (as manifested by calcium deposits and local inflammation in periarticular tissues) has been reported in haemodialyzed (HD) uraemic patients treated with recombinant human erythropoietin. However, short-term treatment with recombinant human erythropoietin (r-Hu EPO) did not influence significantly plasma levels of parathyroid hormone (PTH), calcitonin (CT) and 25-hydroxycholecalciferol (25-OHD3) in uraemic HD patients. The present study aimed to assess the effect of long-term r-Hu EPO therapy for 12 months on plasma PTH, CT, 25-OHD3 and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) in uraemic HD patients.

Adult↗
PubMed1993

Scintillation proximity assay for calcitriol in serum without high pressure liquid chromatography.

A rapid isolation step for 1,25-dihydroxyvitamin D3 without high pressure liquid chromatography (HPLC) and a sensitive radioimmunoassay (RIA) have been developed. The time required for extraction and isolation with a combination of Extrelut-1-minicolumns and Sep-Pak silica cartridges from as little as 0.5 ml serum is only 2 h. The assay can be counted after 8 h of incubation. It is performed in the vial that collects the eluate, thus eliminating transfer losses and errors. No separation of bound and free hormone is necessary before beta-counting in the scintillation proximity assay. The detection limit of the assay is 2.7 ng/l. The intra-assay coefficients of variation are 7.3% and 5.2% for samples with calcitriol concentrations of 31 and 148 ng/l, respectively. The inter-assay coefficients of variation are 11.3%, 13.3% and 16.1% for low (16 ng/l), medium (30 ng/l) and high (148 ng/l) control pool samples, respectively. Normal values for calcitriol range from 32 to 80 ng/l. Elderly subjects, patients with reduced kidney function and pregnant women were also evaluated for their calcitriol levels. This assay correlates well with a RIA employing HPLC prepurification and charcoal separation of bound/free calcitriol (r = 0.94).

Adult↗
PubMed1993

[Diagnostic significance of parathyroid hormone-related protein in tumor patients with hypercalcemia].

The clinical utility of measuring parathormone-related protein (PTHrP) was investigated in 94 patients (48 men, 46 women, mean age 56 [18-82] years) with tumour-associated hypercalcaemia, using a radioimmunoassay directed against the middle portion (53-84) of PTHrP (reference range < 5-21 pmol/l). Increased levels of the middle portion of PTHrP were found in 44 of the 73 patients (60%) with hypercalcaemia associated with solid tumours (median 49 [22-333] pmol/l). There was a positive correlation between the serum calcium concentration and the PTHrP (P = 0.018). The frequency of a raised PTHrP, indicating hormone-induced hypercalcaemia, was similar in patients with and without bone metastases (48% vs 66%). Elevated PTHrP was particularly frequent in patients with squamous cell carcinomas (17 out of 21; 81%), while PTHrP levels were normal in 18 out of the 21 patients with hypercalcaemia associated with haematological malignancies. PTHrP levels were normal in 37 out of 38 normocalcaemic tumour patients and in 30 out of 32 patients with primary hyperparathyroidism. Hypercalcaemia associated with benign disease was found in only one case, a female with marked benign breast hypertrophy.--The measurement of PTHrP allows the demonstration of a pathogenetic factor in tumour-associated hypercalcaemia, and differentiation from other causes of hypercalcaemia, in particular primary hyperparathyroidism.

Adolescent↗
PubMed1993

Somatostatin-receptor imaging of neuroendocrine gastroenteropancreatic tumors.

BACKGROUND: Gastroenteropancreatic neuroendocrine tumors are often difficult to localize. This study was conducted to examine the value of somatostatin-receptor scintigraphy for visualization of gastroenteropancreatic neuroendocrine tumors. METHODS: Applying the recently developed indium-labeled somatostatin analogue 111In-pentetreotide to 40 patients with gastroenteropancreatic neuroendocrine tumors, the diagnostic power of pentreotide-receptor scintigraphy was evaluated in comparison with conventional imaging techniques. RESULTS: Expression of somatostatin receptors was observed in the majority of patients (11 of 17 in the foregut, 14 of 16 in the midgut, and 7 of 7 in metastatic neuroendocrine tumors with unknown primary). Comparative imaging by computerized tomography, magnetic resonance imaging, and transabdominal ultrasonography yielded false-negative results for somatostatin-receptor scintigraphy in 8 of 40 patients; however, in 16 patients, tumor tissue that had escaped conventional imaging techniques was detected by 111In-pentetreotide scintigraphy. CONCLUSIONS: 111In-pentetreotide scintigraphy is a practical, safe, and sensitive procedure for in vivo imaging of gastroenteropancreatic neuroendocrine tumors.

Adolescent↗
PubMed1993

Intermittent versus continuous administration of 1,25-dihydroxyvitamin D3 in experimental renal hyperparathyroidism.

Conflicting results have been reported regarding the efficacy of intermittent versus continuous administration of 1,25(OH)2D3 in renal secondary hyperparathyroidism. To address this issue we examined sham-operated control rats and hyperparathyroid rats with subtotal (5/6) nephrectomy (Nx). The Nx animals (20 to 22 animals per group) were subjected to three treatment protocols: (i) solvent treatment (Nx-solvent); (ii) two i.p. injections of 35 pmol 1,25(OH)2D3 on days 0 and 4 (Nx-bolus); and (iii) continuous infusion of 70 pmol 1,25(OH)2D3 over six days via osmotic minipump (Nx-infusion). All measurements were performed six days after start of treatment. As compared to sham-operated controls, the pre-pro-PTH/beta-actin mRNA ratio was 2.04-fold higher in Nx-solvent. Both modes of administration of 1,25(OH)2D3 resulted in inhibition of PTH mRNA concentrations relative to Nx-solvent. The pre-pro-PTH/beta-actin mRNA ratio was, however, significantly lower (P < 0.05) in Nx-bolus than in Nx-infusion (Nx-bolus 1.26 higher than sham-operated controls; Nx-infusion 1.65 higher than sham-operated controls). Aminoterminal PTH (N-PTH) serum concentrations were higher in Nx-solvent (52 +/- 4 pg/ml) than in sham-operated controls (32 +/- 3 pg/ml, P < 0.01). N-PTH concentrations in Nx-bolus (38 +/- 4 pg/ml) were significantly lower than in Nx-solvent (P < 0.01) and in Nx-infusion (46 +/- 4 pg/ml, P < 0.05). Parathyroid gland weight (microgram/g body wt) was higher in Nx-solvent (1.30 +/- 0.08 pg/ml) than in sham-operated controls (0.79 +/- 0.04 pg/ml, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The mechanism involved in the central effect of 5-leu enkephalin on the calcitonin secretion.

Calcitonin (CT) secretion is not exclusively under the control of calcium levels in the plasma, but also depends on the sympathetic-adrenergic tone. In previous experiments we stressed out the possible role played by 5-leu enkephalin (5-LE) in the nervous regulation of the CT secretion. Intracerebroventricular (i.c.v.) 5-LE in doses of 100 micrograms could act at a central level through a mechanism independent from the noradrenergic pathways, since i.c.v. 6-OHDA and propranolol could not interfere with its stimulatory effect on the CT content of the thyroid. In the present experiments, performed in anaesthetized Wistar-Bratislava rats, we studied the involvement of mu and delta receptors in the central effect of 5-LE on the CT content of the thyroids and the CT levels in the plasma. These parameters were measured in parallel, by means of a competitive radioimmunoassay with double antibodies (Peninsula Lab.). 5-LE probably bound to both mu and delta receptors, since its effect on the CT secretion was reversed by 13 micrograms of naloxone (i.c.v.). A partial blockade, comparable to naloxone, was noticed after 382 micrograms of CTOP (i.c.v.), a specific antagonist of the mu receptors--stressing out their involvement in the stimulatory effect of 5-LE on the CT secretion. 250 Ug of ICI 174864 (i.c.v.), a selective antagonist the the delta receptors completely blocked the stimulation induced by 5-LE on the CT secretion to values significantly lower as compared to the controls and even to the sympathectomized group. This suggests the tonic role played by enkephalins in the CT secretion, through the central activation of delta receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗